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Questions and Answers
What is the most common cause of hypercalcemia in a hospital population?
What is the most common cause of hypercalcemia in a hospital population?
Which of the following symptoms is commonly associated with primary hyperparathyroidism?
Which of the following symptoms is commonly associated with primary hyperparathyroidism?
What serum characteristic is typically observed in patients with hypercalcemia associated with malignancy?
What serum characteristic is typically observed in patients with hypercalcemia associated with malignancy?
Which group is most likely to be affected by primary hyperparathyroidism?
Which group is most likely to be affected by primary hyperparathyroidism?
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Which condition is NOT associated with hypercalcemia?
Which condition is NOT associated with hypercalcemia?
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What percentage of calcium in the body is found in bone?
What percentage of calcium in the body is found in bone?
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Which of the following forms of calcium is considered biologically active?
Which of the following forms of calcium is considered biologically active?
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How does acidosis affect calcium binding to albumin?
How does acidosis affect calcium binding to albumin?
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What is the normal range of total extracellular calcium concentration?
What is the normal range of total extracellular calcium concentration?
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What is the primary hormone produced by the parathyroid glands that regulates calcium levels?
What is the primary hormone produced by the parathyroid glands that regulates calcium levels?
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What happens to PTH stimulation when both calcium and magnesium levels are decreased?
What happens to PTH stimulation when both calcium and magnesium levels are decreased?
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What does 'adjusted calcium' account for in clinical measurements?
What does 'adjusted calcium' account for in clinical measurements?
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Why is it important to measure albumin when assessing total calcium levels?
Why is it important to measure albumin when assessing total calcium levels?
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What is a primary cause of hyperphosphatemia?
What is a primary cause of hyperphosphatemia?
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Which condition is associated with severe hypophosphatemia?
Which condition is associated with severe hypophosphatemia?
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What effect does hypomagnesemia have on neuromuscular function?
What effect does hypomagnesemia have on neuromuscular function?
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How is magnesium homeostasis primarily regulated in the body?
How is magnesium homeostasis primarily regulated in the body?
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Which deficiency can lead to hypoparathyroidism?
Which deficiency can lead to hypoparathyroidism?
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What is a common consequence of hypophosphatemia related to enzyme activation?
What is a common consequence of hypophosphatemia related to enzyme activation?
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What can cause hypomagnesemia aside from nutritional insufficiency?
What can cause hypomagnesemia aside from nutritional insufficiency?
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Which treatment for magnesium deficiency can lead to diarrhea?
Which treatment for magnesium deficiency can lead to diarrhea?
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What is the main characteristic of osteoporosis?
What is the main characteristic of osteoporosis?
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Which biochemical marker is commonly utilized to assess osteoblastic activity?
Which biochemical marker is commonly utilized to assess osteoblastic activity?
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What is a major cause of metabolic bone disease in adults?
What is a major cause of metabolic bone disease in adults?
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What is a risk factor for developing osteoporosis?
What is a risk factor for developing osteoporosis?
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Which of the following conditions is primarily associated with vitamin D deficiency in children?
Which of the following conditions is primarily associated with vitamin D deficiency in children?
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What type of bone is commonly described as 'plastic' in Paget’s disease?
What type of bone is commonly described as 'plastic' in Paget’s disease?
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Which of the following reflects the disturbed bone turnover in osteoporosis?
Which of the following reflects the disturbed bone turnover in osteoporosis?
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Which of the following factors plays a role in the pathophysiology of Paget's disease?
Which of the following factors plays a role in the pathophysiology of Paget's disease?
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What is the primary laboratory finding associated with X-Linked Hypophosphatemia (XLH)?
What is the primary laboratory finding associated with X-Linked Hypophosphatemia (XLH)?
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What is a common consequence of untreated X-Linked Hypophosphatemia?
What is a common consequence of untreated X-Linked Hypophosphatemia?
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Which of the following is NOT a first-line test in serum for evaluating calcium disorders?
Which of the following is NOT a first-line test in serum for evaluating calcium disorders?
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Which electrolyte abnormality is commonly associated with rhabdomyolysis?
Which electrolyte abnormality is commonly associated with rhabdomyolysis?
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What symptom is NOT commonly associated with rhabdomyolysis?
What symptom is NOT commonly associated with rhabdomyolysis?
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What is a typical investigation performed to monitor the status of a patient with rhabdomyolysis?
What is a typical investigation performed to monitor the status of a patient with rhabdomyolysis?
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Which treatment is NOT commonly used for rhabdomyolysis?
Which treatment is NOT commonly used for rhabdomyolysis?
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What can cause rapid destruction of skeletal muscle cells, leading to rhabdomyolysis?
What can cause rapid destruction of skeletal muscle cells, leading to rhabdomyolysis?
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Study Notes
Calcium
- Most abundant mineral in the body
- Plays structural, neuromuscular, enzymatic, and signaling roles
- 99% of calcium is found in bone, 1% in extracellular fluid (ECF)
- Calcium balance is maintained between bone, ECF, and kidneys
- Extracellular total calcium levels are tightly controlled: 2.2-2.6 mmol/L
- In plasma, calcium exists mainly bound to albumin (45%) and as free ionized calcium (55%)
- Free ionized calcium is biologically active and is regulated by parathyroid hormone (PTH)
Calcium/Albumin Binding is Dependent on H+
- Binding decreases in acidosis, leading to increased free calcium
- Binding increases in alkalosis, leading to decreased free calcium
Parathyroid Glands
- Four glands located near the thyroid gland
- Regulate calcium homeostasis but not metabolism
- Produce PTH which interacts with vitamin D to increase calcium levels
- Calcium, magnesium, and phosphate levels affect PTH levels:
- Normal calcium levels, low magnesium: mild PTH stimulation
- Decreased calcium and magnesium: decreased PTH
- Increased phosphate levels: decreased calcium and increased PTH
Hypercalcemia
- Most common causes include primary hyperparathyroidism and hypercalcemia of malignancy
Primary Hyperparathyroidism
- Common endocrine disorder caused by adenomas, hyperplasia, and carcinomas
- Most common in postmenopausal women
- Often due to a parathyroid adenoma, resulting in increased PTH levels
- Hypercalcemia and hypophosphatemia occur
- Most individuals are asymptomatic due to calcium stability
- Symptoms include muscle weakness, fatigue, bradycardia, confusion, etc.
Hypercalcemia Associated with Malignancy
- Most common cause of hypercalcemia in hospitalized patients
- Usually due to PTH-related protein (PTHrP) production by a tumor
- PTH is often undetectable in laboratory tests
- Other abnormal lab findings: very low phosphate, very high urine calcium, and low vitamin D
- Clinical features include neurological, gastrointestinal, renal, cardiac, and bone symptoms
Hypercalcemia - Rare Causes
- Calcium therapy
- Excess vitamin D ingestion
- Thiazide diuretics (Excretion of sodium)
- Granulomatous diseases (synthesis of vit. D)
Phosphate
- Abundant anion in the body
- Important component of nucleic acids, mineral strength, and buffer
- Plays key roles in phosphorylation and dephosphorylation of enzymes
- 80% of phosphate is found in bone
- Concentrations in ECF are controlled by the kidneys, with increased excretion by PTH
Hyperphosphatemia
- Increased phosphate concentrations
- Most common cause is renal failure
- Other causes: hypoparathyroidism, cell damage (redistribution), acidosis (buffer), and pseudohypoparathyroidism (genetic disorder causing resistance to PTH)
Hypophosphatemia
- Important for enzyme activation, glycolysis, oxidative metabolism, and transmembrane transport of K+ and Ca+2
- Influences secretion and action of PTH
- Severe hypomagnesemia can lead to hypoparathyroidism and refractory hypocalcemia
Magnesium Homeostasis
- Around 30% of dietary magnesium is absorbed in the small intestine and distributed to tissues
- Largely controlled by the kidneys
- Hypermagnesemia is uncommon, often associated with renal failure or antiacid use
- Hypomagnesemia (magnesium deficiency in serum) has symptoms similar to hypocalcemia, including impaired neuromuscular function and muscle weakness
Hypomagnesemia - Causes
- Commonly associated with nutritional insufficiency
- Other causes: osmotic diuresis, prolonged diuretic use, nasogastric suction, cytotoxic therapy, and proton pump inhibitors
Hypomagnesemia - Diagnosis and Treatment
- Repeated magnesium levels below 0.7 mmol/L indicate intracellular depletion
- Supplementation is available in oral, intramuscular, and intravenous forms
- Oral supplementation often leads to diarrhea
- Parenteral supplementation is necessary in patients with diarrhea or malabsorption
Metabolic Bone Disease
- Disorders of bone structure and function
- Calcium and phosphate levels may be normal, and hypercalcemia or hypocalcemia may not be associated with marked bone changes
- Main types: osteoporosis, osteomalacia/rickets, Paget's disease, and X-linked hypophosphatemia (XLH)
Bone Turnover (metabolism)
- Bone is constantly broken down and reformed (bone remodeling) by osteoblasts and osteoclasts
- Biochemical markers help assess disease and monitor treatment:
- Urinary hydroxyproline (collagen breakdown)
- Deoxypyridinoline (specific collagen product)
- Alkaline phosphatase (ALP)
- Osteocalcin (sensitive indicator of osteoblastic activity)
Osteoporosis
- Most common bone disorder
- Major cause of morbidity and mortality in the elderly
- Bone turnover favors resorption
- Characterized by low bone mineral density (BMD) and deterioration of bone microarchitecture
- Increased susceptibility to fracture
Osteoporosis - Risk Factors
- Non-modifiable: age, menopause, family history, genetic factors
- Modifiable: diet, smoking, sedentary lifestyle, previous fracture, sex hormone deficiencies, alcohol, immobility
Osteoporosis - Diagnosis and Treatment
- Clinical history and risk factor assessment
- Bone density measurement (bone scan) is essential for diagnosis
- Treatment includes oral bisphosphonates to inhibit osteoclastic function
Osteomalacia and Rickets
- Defective or inadequate bone mineralization
- Osteomalacia affects adults, while rickets affects children (deformities in growing bones)
- Primarily due to vitamin D deficiency (inadequate ingestion or sun exposure)
Osteomalacia and Rickets - Laboratory Considerations
- Low serum calcium
- Increased PTH
- Increased renal phosphate excretion
- Low serum phosphate
- Increased serum ALP
- Symptoms include muscle aches and bone pain
Paget’s Disease of Bone
- Increased osteoclastic and osteoblastic activity (disorganized)
- Common in the elderly
- Causes may be viral or genetic
- Often asymptomatic
Paget’s Disease of Bone - Laboratory Considerations
- No disturbance in serum calcium levels
- Very high serum ALP
- Elevated urinary hydroxyproline
X-Linked Hypophosphatemia (XLH)
- Rare genetic disorder
- Excess phosphate excretion by kidneys
- Decreased phosphate absorption in intestines
- Low phosphate levels in serum
X-Linked Hypophosphatemia (XLH) - Consequences
- Rickets, osteomalacia, short stature, bone/joint pain, and dental problems
- Treatment includes phosphate and active vitamin D supplementation
Calcium Disorders or Bone Disease - Biochemistry Testing
- First line serum tests: calcium, albumin, phosphate, ALP
- Follow-up tests: PTH, magnesium, 25-hydroxycholecalciferol, urine calcium excretion, specific markers of bone turnover
Skeletal Muscle Disorders (Myopathies)
- Conditions leading to muscle weakness or atrophy
- Causes: congenital (muscular dystrophies), infections, anoxia, toxins, drugs, muscle denervation, lack of energy molecules, severe electrolyte imbalance
- Severe damage to muscle cells leads to rhabdomyolysis, releasing myoglobin and creatine kinase (CK)
Rhabdomyolysis
- Rapid destruction of skeletal muscle cells, often due to injury
- Releases large quantities of myoglobin, which can be toxic to the kidneys
- Causes: medications, heatstroke, alcohol & drug use
- Symptoms: muscle weakness, muscle pain, dark urine
- Complications: renal failure, disseminated intravascular coagulation, electrolyte abnormalities (hyperkalemia, hyperphosphatemia, and hypocalcemia)
Rhabdomyolysis - Investigation and Treatment
- Increased serum total CK levels
- Monitoring of urea, electrolytes, alcohol and drug of abuse
- Treatment: cardiac monitoring, electrolyte correction, hemodialysis
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Description
This quiz covers the critical roles of calcium in the body, including its structural and signaling functions. It also discusses calcium balance and the regulation of calcium by parathyroid hormone and its interaction with albumin. Test your knowledge on calcium physiology and its homeostasis!