Calcium and phosphate handling US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Calcium and phosphate handling. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Calcium and phosphate handling US Medical PG Question 1: A 65-year-old female with chronic renal failure presents with recent onset of bone pain. Serum analysis reveals decreased levels of calcium and elevated levels of parathyroid hormone. One of the mechanisms driving the elevated PTH is most similar to that seen in:
- A. Decreased functioning of the calcium-sensing receptor (CASR)
- B. Sarcoidosis
- C. Parathyroid adenoma
- D. End stage liver failure
- E. Insufficient Ca intake (Correct Answer)
Calcium and phosphate handling Explanation: ***Insufficient Ca intake***
- **Chronic renal failure** impairs the kidney's ability to activate **vitamin D**, leading to **decreased calcium absorption** from the gut.
- This resulting **hypocalcemia** stimulates the parathyroid glands to increase **PTH secretion** to normalize calcium, a response similar to that seen with insufficient dietary calcium intake.
*Decreased functioning of the calcium-sensing receptor (CASR)*
- A dysfunctional CASR would lead to **hypercalcemia** and inappropriately normal or elevated PTH, as the parathyroid gland would not recognize normal or high calcium levels.
- In chronic renal failure, the primary issue is **hypocalcemia** leading to secondary hyperparathyroidism, not a problem with calcium sensing itself.
*Sarcoidosis*
- Sarcoidosis can cause **hypercalcemia** due to extrarenal production of **1,25-dihydroxyvitamin D** (calcitriol) by activated macrophages.
- This condition would typically lead to **suppressed PTH levels**, which is the opposite of the elevated PTH seen in the patient's case.
*Parathyroid adenoma*
- A parathyroid adenoma causes **primary hyperparathyroidism**, characterized by **hypercalcemia** and inappropriately high PTH levels.
- The patient in the vignette presents with **hypocalcemia**, making primary hyperparathyroidism less likely as the direct cause of the elevated PTH.
*End stage liver failure*
- Liver failure can impair **vitamin D hydroxylation** in the liver, leading to **decreased 25-hydroxyvitamin D** levels.
- While this can contribute to hypocalcemia and elevated PTH (secondary hyperparathyroidism), it is distinct from the primary mechanism in renal failure involving the kidney's crucial role in **1-alpha hydroxylation** of vitamin D.
Calcium and phosphate handling US Medical PG Question 2: Which region of the nephron reabsorbs the highest percentage of filtered bicarbonate?
- A. Collecting duct
- B. Thick ascending limb
- C. Distal tubule
- D. Proximal tubule (Correct Answer)
Calcium and phosphate handling Explanation: ***Proximal tubule***
- The **proximal convoluted tubule (PCT)** reabsorbs approximately 80-90% of the **filtered bicarbonate** through a process involving **carbonic anhydrase** and the **Na+/H+ exchanger**.
- This vital function ensures that the majority of bicarbonate, a key buffer, is returned to the blood to maintain **acid-base balance**.
*Collecting duct*
- While the collecting duct does have the ability to reabsorb and secrete bicarbonate, its contribution is minor compared to the PCT, primarily for fine-tuning acid-base balance.
- Cells in the collecting duct, particularly **Type A intercalated cells**, are important for secreting acid (H+) in acidosis and therefore reabsorbing bicarbonate, but not the bulk of it.
*Thick ascending limb*
- The primary role of the **thick ascending limb** is the reabsorption of **sodium**, **potassium**, and **chloride** to create a concentrated interstitium, not significant bicarbonate reabsorption.
- It is largely impermeable to water and is relatively impermeable to bicarbonate.
*Distal tubule*
- The **distal convoluted tubule (DCT)** reabsorbs a small percentage of filtered bicarbonate, but its main role is regulated reabsorption of **sodium** and **calcium**, and secretion of **potassium** and **hydrogen ions**.
- Its contribution to bicarbonate reabsorption is much less significant than that of the proximal tubule.
Calcium and phosphate handling US Medical PG Question 3: A 55-year-old man with long-standing diabetes presents with a fragility fracture. He has chronic renal failure secondary to his diabetes. His serum parathyroid hormone concentration is elevated. You measure his serum concentration of 25(OH)-vitamin D and find it to be normal, but his concentration of 1,25(OH)-vitamin D is decreased. Which of the following represents a correct pairing of his clinical condition and serum calcium level?
- A. Secondary hyperparathyroidism with elevated serum calcium
- B. Primary hyperparathyroidism with low serum calcium
- C. Tertiary hyperparathyroidism with low serum calcium
- D. Secondary hyperparathyroidism with low serum calcium (Correct Answer)
- E. Primary hyperparathyroidism with elevated serum calcium
Calcium and phosphate handling Explanation: ***Secondary hyperparathyroidism with low serum calcium***
- **Chronic renal failure** leads to reduced 1-alpha hydroxylation in the kidneys, decreasing the conversion of 25(OH)-vitamin D to its active form, **1,25(OH)-vitamin D**.
- This **decrease in active vitamin D** impairs intestinal calcium absorption and causes resistance to PTH in bone, resulting in **hypocalcemia**, which then stimulates the parathyroid glands to produce more PTH, leading to **secondary hyperparathyroidism**.
*Secondary hyperparathyroidism with elevated serum calcium*
- In secondary hyperparathyroidism due to chronic renal failure, the aim is to correct **hypocalcemia**, so a persistently elevated serum calcium would suggest a different or progressing pathology, such as tertiary hyperparathyroidism.
- While PTH is elevated, it is primarily trying to normalize calcium, which is typically low or low-normal, not elevated, in uncomplicated secondary hyperparathyroidism.
*Primary hyperparathyroidism with low serum calcium*
- **Primary hyperparathyroidism** is characterized by excessive PTH production from a parathyroid adenoma or hyperplasia and typically results in **hypercalcemia**, not low serum calcium.
- The elevated PTH in primary hyperparathyroidism is autonomous, not provoked by hypocalcemia, and would also lead to elevated 1,25(OH)-vitamin D levels.
*Tertiary hyperparathyroidism with low serum calcium*
- **Tertiary hyperparathyroidism** occurs when prolonged secondary hyperparathyroidism leads to autonomous PTH secretion, often resulting in **hypercalcemia**, not hypocalcemia, despite the underlying renal failure.
- This option incorrectly pairs tertiary hyperparathyroidism with low serum calcium; the key feature of tertiary hyperparathyroidism is the emancipation of PTH secretion from calcium regulation.
*Primary hyperparathyroidism with elevated serum calcium*
- While **primary hyperparathyroidism** typically presents with elevated serum calcium, this patient has **chronic renal failure** and a decreased 1,25(OH)-vitamin D, which points to a renal etiology for the calcium imbalance.
- In primary hyperparathyroidism, 1,25(OH)-vitamin D levels would generally be normal or elevated due to PTH stimulation of renal 1-alpha hydroxylase, which contradicts the patient's decreased levels.
Calcium and phosphate handling US Medical PG Question 4: Which factor most strongly influences protein filtration at the glomerulus?
- A. Electrical charge
- B. Molecular size (Correct Answer)
- C. Shape
- D. Temperature
Calcium and phosphate handling Explanation: ***Molecular size***
- The glomerular filtration barrier, particularly the **slit diaphragms** between podocytes, acts as a size-selective filter, restricting the passage of larger molecules.
- Proteins like **albumin** (molecular radius ~36 Å, molecular weight ~69 kDa) are significantly large, making them difficult to pass through the filtration barrier.
- Size selectivity is the **primary and most important** factor in protein filtration.
*Electrical charge*
- The glomerular basement membrane contains **negatively charged proteoglycans** (heparan sulfate), which repel negatively charged proteins like albumin, contributing to their retention.
- While important, the role of electrical charge is **secondary** to molecular size in preventing the bulk passage of most proteins.
*Shape*
- While abnormal protein shapes (e.g., **amyloid fibrils**) can impact filtration in specific disease states, the typical physiological filtration of most proteins is primarily governed by size and charge.
- The inherent shape of normal globular proteins plays a less direct role compared to their overall size.
*Temperature*
- **Physiological temperature** is relatively constant in the body and does not directly influence the molecular interactions and physical properties of the glomerular filtration barrier in a way that significantly alters protein filtration.
- Temperature changes would lead to denaturation or aggregation, which are not the primary determinants of normal protein filtration.
Calcium and phosphate handling US Medical PG Question 5: An investigator is studying the effects of hyperphosphatemia on calcium homeostasis. A high-dose phosphate infusion is administered intravenously to a healthy subject over the course of 3 hours. Which of the following sets of changes is most likely to occur in response to the infusion?
$$$ Serum parathyroid hormone %%% Serum total calcium %%% Serum calcitriol %%% Urine phosphate $$$
- A. ↑ ↓ ↓ ↑
- B. ↓ ↑ ↑ ↓
- C. ↑ ↑ ↑ ↑
- D. ↓ ↓ ↓ ↓
- E. ↑ ↑ ↑ ↓
- F. ↑ ↓ ↑ ↑ (Correct Answer)
Calcium and phosphate handling Explanation: ***↑ ↓ ↑ ↑***
- A high-dose phosphate infusion causes **hyperphosphatemia**, which leads to binding of ionized calcium and results in **hypocalcemia** (decreased serum total calcium).
- The hypocalcemia stimulates the parathyroid glands to secrete **increased PTH**.
- Elevated PTH stimulates 1α-hydroxylase in the kidneys, leading to **increased calcitriol** (active vitamin D) production to enhance intestinal calcium absorption and renal calcium reabsorption.
- Both the high filtered load of phosphate and **PTH's phosphaturic effect** lead to **increased urinary phosphate excretion** as the kidneys attempt to restore phosphate balance.
*↑ ↓ ↓ ↑*
- This option correctly predicts increased PTH and increased urinary phosphate, but incorrectly suggests **decreased calcitriol**.
- PTH stimulation would increase 1α-hydroxylase activity, leading to **increased calcitriol production**, not decreased.
*↓ ↑ ↑ ↓*
- This option incorrectly predicts **decreased PTH** following hyperphosphatemia.
- Hyperphosphatemia causes hypocalcemia, which **stimulates PTH release**, not suppresses it.
- An increase in serum total calcium is also incorrect, as phosphate binds calcium acutely.
*↑ ↑ ↑ ↑*
- While this option correctly predicts increased PTH and calcitriol, it incorrectly suggests **increased serum total calcium**.
- Acute hyperphosphatemia causes calcium-phosphate binding, leading to **decreased ionized and total calcium**, which is the trigger for PTH release.
- However, urinary phosphate would correctly increase in this scenario.
*↓ ↓ ↓ ↓*
- This option is completely incorrect as it suggests all parameters decrease.
- Hyperphosphatemia triggers compensatory mechanisms including **increased PTH and calcitriol**, not decreases.
- Urinary phosphate must **increase** to excrete the excess phosphate load, not decrease.
*↑ ↑ ↑ ↓*
- This option incorrectly combines increased serum total calcium with **decreased urinary phosphate**.
- In hyperphosphatemia, urinary phosphate excretion **must increase** due to both the filtered load and PTH's phosphaturic effect.
- Additionally, acute phosphate binding would **decrease** serum calcium initially, though compensatory mechanisms attempt to restore it.
Calcium and phosphate handling US Medical PG Question 6: In a healthy patient with no renal abnormalities, several mechanisms are responsible for moving various filtered substances into and out of the tubules. Para-aminohippurate (PAH) is frequently used to estimate renal blood flow when maintained at low plasma concentrations. The following table illustrates the effect of changing plasma PAH concentrations on PAH excretion:
Plasma PAH concentration (mg/dL) | Urinary PAH concentration (mg/dL)
0 | 0
10 | 60
20 | 120
30 | 150
40 | 180
Which of the following mechanisms best explains the decreased rate of increase in PAH excretion observed when plasma PAH concentration exceeds 20 mg/dL?
- A. Decreased glomerular filtration of PAH
- B. Increased rate of PAH reabsorption
- C. Increased flow rate of tubular contents
- D. Saturation of PAH transport carriers (Correct Answer)
- E. Increased diffusion rate of PAH
Calcium and phosphate handling Explanation: ***Saturation of PAH transport carriers***
- PAH is primarily cleared by **tubular secretion** via organic anion transporters (OATs) in the proximal tubule, which have a **finite transport maximum (Tm)**.
- When plasma PAH concentration exceeds the capacity of these carriers (as seen above 20 mg/dL), the transporters become saturated, leading to a **decreased incremental excretion** despite rising plasma levels.
*Decreased glomerular filtration of PAH*
- **Glomerular filtration rate (GFR)** for PAH is proportional to its plasma concentration and is typically constant in a healthy kidney, so it would not decrease with increasing plasma PAH.
- A decrease in GFR would lead to a *reduced* overall excretion, but not specifically explain the *decreased rate of increase* at higher plasma concentrations.
*Increased rate of PAH reabsorption*
- PAH is **minimally reabsorbed** in the renal tubules; its primary mechanism of removal from the blood is active secretion.
- An increase in reabsorption would lead to *less* PAH in the urine, but there's no physiological basis for increased reabsorption as plasma concentration rises.
*Increased flow rate of tubular contents*
- While an increased flow rate can sometimes affect solute reabsorption or secretion, it would generally lead to a more, not less, efficient clearance of secreted substances.
- This mechanism does not explain the **saturation kinetics** observed with PAH at higher plasma concentrations.
*Increased diffusion rate of PAH*
- PAH is a charged organic anion, and its movement across tubular membranes is primarily mediated by **active transport** rather than simple diffusion.
- Even if diffusion played a minor role, an increased diffusion rate would generally lead to *more* excretion, not the observed plateau in the rate of increase.
Calcium and phosphate handling US Medical PG Question 7: An investigator is studying membranous transport proteins in striated muscle fibers of an experimental animal. An electrode is inserted into the gluteus maximus muscle and a low voltage current is applied. In response to this, calcium is released from the sarcoplasmic reticulum of the muscle fibers and binds to troponin C, which results in a conformational change of tropomyosin and unblocking of the myosin-binding site. The membranous transport mechanism underlying the release of calcium into the cytosol most resembles which of the following processes?
- A. Opening of acetylcholine receptors at neuromuscular junction
- B. Reabsorption of glucose by renal tubular cells
- C. Secretion of doxorubicin from dysplastic colonic cells
- D. Uptake of fructose by small intestinal enterocytes (Correct Answer)
- E. Removal of calcium from cardiac myocytes
Calcium and phosphate handling Explanation: **Uptake of fructose by small intestinal enterocytes**
- The release of calcium from the sarcoplasmic reticulum into the cytosol in muscle contraction is primarily mediated by **ryanodine receptors**, which are a type of **facilitated diffusion channel**.
- **Fructose uptake** in the small intestine occurs via **GLUT5 transporters**, which also utilize **facilitated diffusion**, moving fructose down its concentration gradient without direct energy expenditure.
*Opening of acetylcholine receptors at neuromuscular junction*
- The opening of **acetylcholine receptors** is a form of **ligand-gated ion channel** activity, specific to the binding of acetylcholine.
- While it involves channel opening, it's initiated by a chemical signal, whereas sarcoplasmic reticulum calcium release is often voltage-gated or mechanically coupled to voltage sensors.
*Reabsorption of glucose by renal tubular cells*
- Glucose reabsorption in renal tubules primarily involves **secondary active transport** via **SGLT transporters**, which co-transport glucose with sodium.
- This process requires energy indirectly, unlike the facilitated diffusion of calcium from the sarcoplasmic reticulum.
*Secretion of doxorubicin from dysplastic colonic cells*
- The secretion of doxorubicin, an anticancer drug, from cells often involves **ATP-binding cassette (ABC) transporters** (e.g., MDR1), which utilize **primary active transport** to pump substances against their concentration gradient using ATP.
- This is an energy-dependent process, distinct from facilitated diffusion.
*Removal of calcium from cardiac myocytes*
- The removal of calcium from cardiac myocytes occurs primarily via the **SERCA pump** (an **ATP-dependent active transporter**) back into the sarcoplasmic reticulum and the **Na+/Ca2+ exchanger** (a **secondary active transporter**) out of the cell.
- Both mechanisms require energy, either directly or indirectly, to move calcium against its electrochemical gradient.
Calcium and phosphate handling US Medical PG Question 8: A 52-year-old man comes to the physician because of a 4-month history of fatigue, weakness, constipation, decreased appetite, and intermittent flank pain. He takes ibuprofen for knee and shoulder pain. Physical examination shows mild tenderness bilaterally in the costovertebral areas. His serum calcium concentration is 11.2 mg/dL, phosphorus concentration is 2.5 mg/dL, and N-terminal parathyroid hormone concentration is 830 pg/mL. Which of the following steps in vitamin D metabolism is most likely increased in this patient?
- A. Ergocalciferol → 25-hydroxyergocalciferol
- B. 7-dehydrocholesterol → cholecalciferol
- C. 25-hydroxycholecalciferol → 1,25-dihydroxycholecalciferol (Correct Answer)
- D. 25-hydroxycholecalciferol → 24,25-dihydroxycholecalciferol
- E. Cholecalciferol → 25-hydroxycholecalciferol
Calcium and phosphate handling Explanation: ***25-hydroxycholecalciferol → 1,25-dihydroxycholecalciferol***
- This patient presents with **hypercalcemia** (11.2 mg/dL), **hypophosphatemia** (2.5 mg/dL), and a markedly **elevated N-terminal parathyroid hormone (PTH)** concentration (830 pg/mL), which are classic findings for **primary hyperparathyroidism**.
- In primary hyperparathyroidism, elevated PTH directly stimulates the **renal 1-alpha-hydroxylase enzyme**, increasing the conversion of **25-hydroxycholecalciferol** (calcidiol) to its active form, **1,25-dihydroxycholecalciferol** (calcitriol), which raises calcium levels.
*Ergocalciferol → 25-hydroxyergocalciferol*
- This step involves the **hepatic 25-hydroxylase enzyme** converting dietary vitamin D2 (ergocalciferol) to its storage form, which is not primarily regulated by PTH in the context of hyperparathyroidism.
- While essential for vitamin D activation, this conversion rate is usually adequate and not the primary increased step responsible for the hypercalcemic state in this patient's presentation.
*7-dehydrocholesterol → cholecalciferol*
- This process is the **cutaneous synthesis of vitamin D3 (cholecalciferol)**, which is dependent on UV light exposure and is not directly regulated by PTH.
- This initial step of vitamin D synthesis occurs in the skin and is upstream of the metabolic pathway influenced by PTH.
*25-hydroxycholecalciferol → 24,25-dihydroxycholecalciferol*
- This conversion produces an **inactive form of vitamin D** and is catalyzed by the **24-hydroxylase enzyme**.
- This enzyme activity is typically **suppressed by high PTH** and **increased by high levels of 1,25-dihydroxycholecalciferol**, serving to degrade excess active vitamin D; therefore, this step would likely be decreased, not increased, in primary hyperparathyroidism.
*Cholecalciferol → 25-hydroxycholecalciferol*
- This is the **hepatic 25-hydroxylation** of vitamin D3, producing 25-hydroxycholecalciferol (calcidiol), the major circulating form of vitamin D.
- While critical for producing the substrate for further activation, this step is not the *most likely increased* step in response to high PTH in primary hyperparathyroidism.
Calcium and phosphate handling US Medical PG Question 9: A 28-year-old man comes to the physician for a follow-up examination after a previous visit showed an elevated serum calcium level. He has a history of bipolar disorder. His mother had a parathyroidectomy in her 30s. The patient does not drink alcohol or smoke. Current medications include lithium and a daily multivitamin. His vital signs are within normal limits. Physical examination shows no abnormalities. Laboratory studies show:
Serum
Sodium 146 mEq/L
Potassium 3.7 mEq/L
Calcium 11.2 mg/dL
Magnesium 2.3 mEq/L
PTH 610 pg/mL
Albumin 4.2 g/dL
24-hour urine
Calcium 23 mg
Which of the following is the most likely cause of this patient’s findings?
- A. Lithium toxicity
- B. Parathyroid adenoma
- C. Excess calcium intake
- D. Excess vitamin D intake
- E. Abnormal calcium sensing receptors (Correct Answer)
Calcium and phosphate handling Explanation: ***Abnormal calcium sensing receptors***
- The patient's **hypocalciuric hypercalcemia** (high serum calcium, low urine calcium) in the presence of an **elevated PTH** suggests a defect in calcium sensing.
- The family history of parathyroidectomy in the mother is consistent with an inherited condition affecting **calcium-sensing receptors (CaSRs)**, such as **familial hypocalciuric hypercalcemia (FHH)**.
*Lithium toxicity*
- **Lithium** can cause hypercalcemia by increasing the set point for calcium at the parathyroid gland, leading to increased PTH secretion.
- However, lithium typically does not lead to **hypocalciuria** to the extent seen in FHH, as it does not directly affect the kidney's CaSR in the same manner.
*Parathyroid adenoma*
- A **parathyroid adenoma** would cause **primary hyperparathyroidism**, characterized by hypercalcemia and elevated PTH.
- However, primary hyperparathyroidism typically presents with **hypercalciuria** due to the PTH-mediated increase in renal calcium reabsorption being overwhelmed by the increased filtered calcium load, unlike the hypocalciuria seen here.
*Excess calcium intake*
- **Excess calcium intake** could lead to hypercalcemia, but this would typically suppress PTH (unless it's a milk-alkali syndrome variant).
- It would also lead to **hypercalciuria** as the kidneys attempt to excrete the excess calcium, which is not observed here with a suppressed 24-hour urine calcium.
*Excess vitamin D intake*
- **Excess vitamin D intake** causes hypercalcemia by increasing intestinal calcium absorption and bone resorption, and would typically lead to **suppressed PTH** levels.
- It would also typically result in **hypercalciuria** due to the increased filtered calcium load, contrasting with the low urine calcium in this patient.
Calcium and phosphate handling US Medical PG Question 10: A 17-year-old boy is brought to the physician by his father because of a 7-month history of fatigue, recurrent leg cramps, and increased urinary frequency. His pulse is 94/min and blood pressure is 118/85 mm Hg. Physical examination shows dry mucous membranes. Laboratory studies show:
Serum
Na+ 130 mEq/L
K+ 2.8 mEq/L
Cl- 92 mEq/L
Mg2+ 1.1 mEq/L
Ca2+ 10.6 mg/dL
Albumin 5.2 g/dL
Urine
Ca2+ 70 mg/24 h
Cl- 375 mEq/24h (N = 110–250)
Arterial blood gas analysis on room air shows a pH of 7.55 and an HCO3- concentration of 45 mEq/L. Impaired function of which of the following structures is the most likely cause of this patient's condition?
- A. Ascending loop of Henle
- B. Collecting duct
- C. Distal convoluted tubule (Correct Answer)
- D. Descending loop of Henle
- E. Proximal convoluted tubule
Calcium and phosphate handling Explanation: ***Distal convoluted tubule***
- The patient presents with **hypokalemia**, **metabolic alkalosis**, **hypomagnesemia**, and **hypocalciuria** (24-hour urine Ca2+ 70 mg, normal up to 250 mg), which are characteristic findings of **Gitelman syndrome**.
- **Gitelman syndrome** is caused by a loss-of-function mutation in the **thiazide-sensitive Na-Cl cotransporter (NCC)**, located in the **distal convoluted tubule**, leading to impaired reabsorption of Na+ and Cl- at this segment.
*Ascending loop of Henle*
- Impaired function of the **Na-K-2Cl cotransporter (NKCC2)** in the **thick ascending limb of the loop of Henle** causes **Bartter syndrome**.
- Bartter syndrome typically presents with **hypercalciuria**, in contrast to the hypocalciuria seen in this patient.
*Collecting duct*
- Dysfunction of the **collecting duct** can lead to various conditions, such as **renal tubular acidosis** or **diabetes insipidus**, depending on which channels or receptors are affected.
- However, the specific combination of **hypokalemia**, **metabolic alkalosis**, **hypomagnesemia**, and **hypocalciuria** points away from primary collecting duct dysfunction.
*Descending loop of Henle*
- The **descending loop of Henle** is primarily permeable to **water** and has a limited role in electrolyte reabsorption.
- Impairment here would primarily affect **urine concentration** and dilution but would not account for the specific electrolyte imbalances observed.
*Proximal convoluted tubule*
- The **proximal convoluted tubule** is responsible for reabsorbing a large fraction of filtered electrolytes, glucose, and amino acids.
- Dysfunction here (e.g., **Fanconi syndrome**) would typically present with **generalized aminoaciduria**, **glycosuria**, **phosphaturia**, and **proximal renal tubular acidosis**, which are not seen in this patient.
More Calcium and phosphate handling US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
