Drugs Affecting Calcium Metabolism — MCQs
Calcium absorption is affected by-
Which of the following is not a treatment option for hypercalcemia?
The function of which of the following is increased by an elevated parathyroid hormone concentration:
Which hormone directly lowers blood calcium levels?
Calcium absorption is increased by
Which drug increases bone formation in osteoporosis?
Which of the following is the drug of choice for the treatment of Syndrome of Inappropriate Antidiuretic Hormone secretion?
Which drug is metabolized by glutathionation?
Which of the following anti-diabetic drugs is associated with increased risk of UTI?
A 24 year old male presents with altered sensorium and rapid shallow breathing. ABG shows:pH 7.2, sodium 140, bicarbonate 10 and chloride 98. Probable diagnosis is -
Drugs Affecting Calcium Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: Calcium absorption is affected by-
- A. Calcitriol
- B. PTH
- C. Proteins
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Calcitriol**, **parathyroid hormone (PTH)**, and **proteins** all play crucial roles in regulating calcium absorption and metabolism. - While calcitriol directly enhances intestinal calcium absorption, PTH indirectly influences it via calcitriol synthesis, and proteins are necessary for calcium transport and binding. *Calcitriol* - **Calcitriol** (1,25-dihydroxyvitamin D3) is the hormonally active form of vitamin D, which is essential for stimulating calcium absorption in the intestine. - It increases the synthesis of **calcium-binding proteins (calbindins)** in enterocytes, facilitating calcium uptake. *PTH* - **Parathyroid hormone (PTH)** primarily regulates calcium levels by stimulating its release from bone and increasing reabsorption in the kidneys. - It also indirectly enhances intestinal calcium absorption by stimulating the **renal conversion of 25-hydroxyvitamin D to calcitriol**. *Proteins* - Various **proteins** are involved in calcium transport and absorption, including calcium-binding proteins (e.g., calbindin) in the gut. - Dietary protein intake can also influence calcium balance; however, specific mechanisms regarding direct absorption are more complex and indirect compared to calcitriol.
Question 2: Which of the following is not a treatment option for hypercalcemia?
- A. Strontium (Correct Answer)
- B. Bisphosphonates
- C. Steroids
- D. Phosphate
Explanation: ***Strontium*** - **Strontium ranelate** is primarily used in the treatment of **osteoporosis** to promote bone formation and inhibit bone resorption. - It does not have a recognized role in the acute or long-term management of **hypercalcemia** and could potentially worsen it due to its bone-targeting effects if not carefully managed. *Steroids* - **Glucocorticoids** are effective in treating hypercalcemia associated with **granulomatous diseases** (e.g., sarcoidosis) and certain malignancies (e.g., multiple myeloma) by reducing calcitriol production or tumor burden. - They decrease intestinal calcium absorption and increase renal calcium excretion in conditions where 1,25-dihydroxyvitamin D is elevated. *Bisphosphonates* - **Bisphosphonates** (e.g., zoledronic acid, pamidronate) are potent inhibitors of **osteoclast-mediated bone resorption** and are a cornerstone in the treatment of moderate to severe hypercalcemia, especially due to malignancy. [1] - They are administered intravenously and act by inducing osteoclast apoptosis, thereby reducing the release of calcium from bone. [1] *Phosphate* - **Intravenous phosphate** can be used in severe, resistant hypercalcemia, as it promotes calcium deposition into bone and soft tissues, and forms insoluble calcium-phosphate complexes, thus lowering serum calcium. - Its use is limited due to risks of **ectopic calcification**, renal failure, and hypotension, and it is usually reserved for life-threatening situations where other treatments have failed.
Question 3: The function of which of the following is increased by an elevated parathyroid hormone concentration:
- A. Action of osteoblasts only
- B. Osteoclasts (Correct Answer)
- C. Phosphate reabsorptive pathways in the renal tubules
- D. Hepatic formation of 25-hydroxycholecalciferol
Explanation: ***Osteoclasts*** - **Parathyroid hormone (PTH)** primarily acts to increase serum calcium levels by stimulating **osteoclasts**, leading to bone resorption and release of calcium and phosphate into the bloodstream. - While PTH does not directly act on osteoclasts, it binds to receptors on osteoblasts, which then release factors that activate osteoclasts. *Action of osteoblasts only* - PTH indirectly affects **osteoblasts** by binding to their receptors, but this action primarily leads to **RANKL expression**, which then stimulates osteoclast activity, not a direct increase in osteoblastic bone formation. - Chronic elevation of PTH, as seen in primary hyperparathyroidism, can paradoxically lead to a net loss of bone mass due to increased osteoclastic activity. *Phosphate reabsorptive pathways in the renal tubules* - PTH actually **decreases reabsorption of phosphate** in the renal tubules, leading to phosphaturia. This helps to prevent calcium-phosphate precipitation by lowering serum phosphate levels while raising calcium. - This is a key mechanism by which PTH increases serum calcium—by both mobilizing it from bone and reducing its renal excretion, while simultaneously promoting renal phosphate excretion. *Hepatic formation of 25-hydroxycholecalciferol* - The **liver** is responsible for the hydroxylation of vitamin D3 (cholecalciferol) to **25-hydroxycholecalciferol (calcidiol)**, a process that is not directly regulated by PTH. - PTH primarily stimulates the **kidneys** to convert 25-hydroxycholecalciferol to its active form, **1,25-dihydroxyvitamin D (calcitriol)**, which then enhances intestinal calcium absorption.
Question 4: Which hormone directly lowers blood calcium levels?
- A. Parathyroid hormone
- B. Calcitonin (Correct Answer)
- C. 1, 25-dihydroxycholecalciferol
- D. Vitamin D
Explanation: ***Calcitonin*** - **Calcitonin** is a hormone secreted by the **parafollicular C cells** of the thyroid gland. - Its primary function is to **lower blood calcium levels** by inhibiting osteoclast activity and promoting calcium excretion by the kidneys. - It is the only hormone that directly acts to **decrease serum calcium**. *Parathyroid hormone* - **PTH** is secreted by the parathyroid glands and has the **opposite effect** to calcitonin. - It **increases blood calcium levels** by stimulating osteoclast activity, increasing renal calcium reabsorption, and activating vitamin D. *1,25-dihydroxycholecalciferol* - This is the **active form of vitamin D**, also known as **calcitriol**. - Its main roles are to **increase blood calcium levels** by enhancing calcium absorption from the intestine and promoting bone resorption. *Vitamin D* - **Vitamin D** (cholecalciferol or ergocalciferol) is a precursor that needs to be metabolized into its active form, 1,25-dihydroxycholecalciferol. - Its ultimate effect (via its active form) is to **raise blood calcium levels**, not lower them.
Question 5: Calcium absorption is increased by
- A. Hypercalcemia
- B. Oxalates in the diet
- C. Iron overload
- D. 1.25 Dihydrocholecalciferol (Correct Answer)
Explanation: ***1.25 Dihydrocholecalciferol*** - **1,25-dihydroxycholecalciferol** (calcitriol), the active form of vitamin D, plays a crucial role in **calcium homeostasis** by enhancing calcium absorption from the intestine. - This hormone stimulates the synthesis of **calcium-binding proteins** in intestinal epithelial cells, facilitating the uptake and transport of dietary calcium. *Hypercalcemia* - **Hypercalcemia** (high blood calcium levels) **inhibits** the production of parathyroid hormone (PTH) and **reduces the activation of vitamin D**, thereby decreasing calcium absorption. - The body aims to maintain calcium balance, so excessive calcium in the blood would trigger mechanisms to reduce further absorption, not increase it. *Oxalates in the diet* - **Oxalates** (found in foods like spinach and rhubarb) bind to calcium in the gut to form **insoluble calcium oxalate**, which cannot be absorbed. - This binding effectively **reduces the bioavailability** of dietary calcium, making it less available for absorption. *Iron overload* - **Iron overload** primarily affects iron metabolism and storage, with limited direct impact on calcium absorption mechanisms. - While excessive iron can have systemic effects, it does not directly enhance the absorption of calcium from the intestine.
Question 6: Which drug increases bone formation in osteoporosis?
- A. Teriparatide (Correct Answer)
- B. Calcitonin
- C. Risedronate
- D. Denosumab
Explanation: ***Correct Option: Teriparatide*** - **Teriparatide** is a recombinant form of **parathyroid hormone (PTH)** that, when administered intermittently, stimulates **osteoblast activity** to increase bone formation. - It is an **anabolic agent** specifically designed to build new bone, making it unique among osteoporosis treatments that primarily inhibit bone resorption. - Administered as a **daily subcutaneous injection** for up to 2 years. *Incorrect Option: Calcitonin* - **Calcitonin** is a hormone that inhibits **osteoclast activity**, thereby reducing bone resorption, but does not directly stimulate bone formation. - It may be used for pain relief in acute vertebral fractures but has a minor role in increasing bone density. *Incorrect Option: Risedronate* - **Risedronate** is a **bisphosphonate** that works by inhibiting **osteoclast-mediated bone resorption**, preventing bone breakdown. - It does not directly promote new bone formation; its primary action is to reduce bone turnover. *Incorrect Option: Denosumab* - **Denosumab** is a **monoclonal antibody** that targets and binds to **RANKL**, thereby inhibiting **osteoclast formation, function, and survival**, leading to decreased bone resorption. - Like bisphosphonates, its main mechanism is anti-resorptive, not anabolic.
Question 7: Which of the following is the drug of choice for the treatment of Syndrome of Inappropriate Antidiuretic Hormone secretion?
- A. Demeclocycline (Correct Answer)
- B. Chlorpropamide
- C. Vasopressin
- D. Thiazide diuretics
Explanation: ***Demeclocycline*** - **Demeclocycline** is a **tetracycline antibiotic** that inhibits the action of ADH on the renal tubules, promoting excretion of water. - This effect helps to correct the **hyponatremia** and fluid retention seen in SIADH. - It is considered the **classic drug of choice** for chronic SIADH management, though newer agents like vaptans are increasingly used. *Chlorpropamide* - **Chlorpropamide** is a **sulfonylurea** medication primarily used for **type 2 diabetes mellitus** to stimulate insulin release. - It can **potentiate ADH action**, which would worsen SIADH rather than treat it. *Vasopressin* - **Vasopressin** (also known as ADH) is the **hormone** whose excessive secretion is the underlying problem in SIADH. - Administering vasopressin would **aggravate** the condition by increasing water reabsorption and worsening hyponatremia. *Thiazide diuretics* - **Thiazide diuretics** can **worsen hyponatremia** by impairing the kidney's ability to dilute urine and excrete free water. - This makes them **contraindicated in SIADH** management. - They are used in conditions like **hypertension** or paradoxically in **nephrogenic diabetes insipidus** (where they reduce urine output), but not for treating SIADH.
Question 8: Which drug is metabolized by glutathionation?
- A. Nicotinic acid
- B. Fosfomycin
- C. Benzodiazepines
- D. Dapsone (Correct Answer)
Explanation: ***Dapsone***- **Dapsone** undergoes hepatic metabolism via **N-hydroxylation** by CYP450 enzymes (particularly CYP2E1 and CYP3A4), forming reactive **hydroxylamine metabolites**.- These reactive metabolites are toxic and can cause **methemoglobinemia** and **hemolysis**.- **Glutathione conjugation (glutathionation)** serves as an important **detoxification pathway** for these reactive dapsone metabolites [1].- Individuals with **glutathione deficiency** (such as G6PD deficiency) are at increased risk of dapsone-induced hemolytic anemia [2].*Fosfomycin*- **Fosfomycin** is primarily eliminated by the kidneys as an **unchanged drug** (up to 90% excreted unchanged in urine).- It undergoes **minimal hepatic metabolism** and does NOT undergo significant glutathionation.- Its primary route of elimination is **renal excretion** via glomerular filtration.*Benzodiazepines*- **Benzodiazepines** are primarily metabolized in the liver via **CYP450 enzymes** (Phase I oxidation) followed by **glucuronidation** (Phase II conjugation).- They do NOT undergo glutathionation as a significant metabolic pathway.*Nicotinic acid*- **Nicotinic acid** (niacin) undergoes conjugation with **glycine** to form nicotinuric acid and **methylation** to form N-methylnicotinamide.- It does NOT undergo glutathione conjugation.
Question 9: Which of the following anti-diabetic drugs is associated with increased risk of UTI?
- A. Dapagliflozin (Correct Answer)
- B. Pioglitazone
- C. Metformin
- D. Sitagliptin
Explanation: ***Dapagliflozin*** - **Dapagliflozin** is a **sodium-glucose cotransporter-2 (SGLT2) inhibitor** that works by increasing glucose excretion in the urine. - This increased urinary glucose provides a favorable environment for bacterial growth, leading to a higher risk of **urinary tract infections (UTIs)** and **genital mycotic infections**. *Pioglitazone* - **Pioglitazone** is a **thiazolidinedione** that improves insulin sensitivity in peripheral tissues. - Its primary side effects include **fluid retention**, **weight gain**, and increased risk of **bone fractures** and **heart failure**, not UTIs. *Metformin* - **Metformin** is a **biguanide** that reduces hepatic glucose production and improves insulin sensitivity. - Its most common side effects are **gastrointestinal disturbances** like nausea, diarrhea, and abdominal pain, and it does not typically increase the risk of UTIs. *Sitagliptin* - **Sitagliptin** is a **dipeptidyl peptidase-4 (DPP-4) inhibitor** that enhances endogenous incretin hormones, leading to increased insulin release and reduced glucagon secretion. - It is generally well-tolerated, with side effects that can include **nasopharyngitis** and headache, but it is not associated with an increased risk of UTIs.
Question 10: A 24 year old male presents with altered sensorium and rapid shallow breathing. ABG shows:pH 7.2, sodium 140, bicarbonate 10 and chloride 98. Probable diagnosis is -
- A. Amphetamine toxicity
- B. DKA (Correct Answer)
- C. Renal tubular acidosis
- D. Ethylene glycol poisoning
Explanation: ***DKA*** - The patient presents with **altered sensorium** and **rapid shallow breathing** (Kussmaul breathing), consistent with severe metabolic acidosis [1]. - The ABG results show **pH 7.2** (acidosis), **bicarbonate 10** (metabolic component), and an **elevated anion gap** (Na - (Cl + HCO3) = 140 - (98 + 10) = 32), which are characteristic findings in **diabetic ketoacidosis (DKA)** [1], [2]. *Amphetamine toxicity* - Amphetamine toxicity typically causes **sympathomimetic effects** such as tachycardia, hypertension, hyperthermia, and agitation, rather than directly leading to a high anion gap metabolic acidosis of this severity. - While it can cause some metabolic derangements, the primary acid-base disturbance is usually different or less pronounced in this manner compared to DKA. *Renal tubular acidosis* - Renal tubular acidosis (RTA) typically presents with a **normal anion gap metabolic acidosis** (hyperchloremic metabolic acidosis), where the anion gap would not be significantly elevated. - The calculated anion gap of 32 in this patient rules out RTA as the primary cause of this severe acidosis. *Ethylene glycol poisoning* - Ethylene glycol poisoning also causes a **high anion gap metabolic acidosis** and altered mental status. - However, it is typically associated with additional specific symptoms like **flank pain**, **oliguria**, and detection of **calcium oxalate crystals** in the urine, which are not mentioned in this case.
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