Renal Osteodystrophy — MCQs

10 questions

In hypoparathyroidism:

The primary pharmacological intervention to retard avascular necrosis progression is?

A 10-year-old boy has a fracture of the femur. Biochemical evaluation revealed a hemoglobin level of 11.5 g/dL and an erythrocyte sedimentation rate of 18 mm in the first hour. Serum calcium levels were 12.8 mg/dL, serum phosphorus levels were 2.3 mg/dL, alkaline phosphatase levels were 28 KA units, and blood urea levels were 32 mg/dL. Which of the following is the most probable diagnosis in his case?

What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?

A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?

A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -

False about Marble bone disease

Marble bone disease is:

The following gait is seen due to weakness of:

Q10

The commonest complication of fracture of clavicle is :

Renal Osteodystrophy Indian Medical PG Practice Questions and MCQs

Question 1: In hypoparathyroidism:

A. Plasma calcium is high and inorganic phosphorous low
B. Plasma calcium and inorganic phosphorous are low
C. Plasma calcium is low and inorganic phosphorous high (Correct Answer)
D. Plasma calcium and inorganic phosphorous are high

Explanation: ***Plasma calcium is low and inorganic phosphorous high*** - **Hypoparathyroidism** is characterized by insufficient parathyroid hormone (PTH) production, leading to decreased bone resorption and reduced renal reabsorption of calcium [1]. This results in **hypocalcemia** (low plasma calcium) [1]. - PTH also promotes renal excretion of phosphate [2]. With insufficient PTH, renal phosphate excretion is impaired, leading to **hyperphosphatemia** (high inorganic phosphorus) [1]. *Plasma calcium is high and inorganic phosphorous low* - This profile is characteristic of **primary hyperparathyroidism**, where excessive PTH causes increased bone resorption and renal calcium reabsorption (high calcium), and increased renal phosphate excretion (low phosphorus). - It directly contradicts the defining features of hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are low* - While plasma calcium is low in hypoparathyroidism, plasma inorganic phosphorus is characteristically high, not low [1]. - A combination of low calcium and low phosphorus can be seen in conditions like **vitamin D deficiency** (osteomalacia), but not directly in pure hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are high* - This combination of high calcium and high phosphorus is uncommon and not typically seen in either hypoparathyroidism or hyperparathyroidism. - It could potentially indicate conditions like **milk-alkali syndrome** or **vitamin D intoxication**, but not hypoparathyroidism, which is defined by low calcium [1].

Question 2: The primary pharmacological intervention to retard avascular necrosis progression is?

A. High-dose calcium supplementation
B. Vitamin D supplementation alone
C. Corticosteroid therapy
D. Bisphosphonates (Alendronate) (Correct Answer)

Explanation: ***Bisphosphonates (Alendronate)*** - **Bisphosphonates** inhibit osteoclast-mediated bone resorption and reduce bone cell death, showing promise in preventing progression of early-stage **avascular necrosis**. [1] - Alendronate specifically has been studied for its **bone-preserving effects** in AVN by maintaining bone architecture and potentially slowing femoral head collapse. *Corticosteroid therapy* - **Corticosteroids** are a major **risk factor** for developing avascular necrosis, not a treatment for it. - They cause AVN through mechanisms including **fat embolism**, increased **intraosseous pressure**, and direct **osteocyte toxicity**. *High-dose calcium supplementation* - **Calcium supplementation** supports general bone health but does not address the underlying **vascular disruption** in AVN. - No evidence exists that calcium alone can retard **AVN progression**, which involves interruption of blood supply leading to bone death. *Vitamin D supplementation alone* - **Vitamin D** is essential for calcium absorption and bone mineralization but does not target **AVN pathophysiology**. - Like calcium, it does not address the primary mechanism of **blood supply disruption** that characterizes avascular necrosis.

Question 3: A 10-year-old boy has a fracture of the femur. Biochemical evaluation revealed a hemoglobin level of 11.5 g/dL and an erythrocyte sedimentation rate of 18 mm in the first hour. Serum calcium levels were 12.8 mg/dL, serum phosphorus levels were 2.3 mg/dL, alkaline phosphatase levels were 28 KA units, and blood urea levels were 32 mg/dL. Which of the following is the most probable diagnosis in his case?

A. Renal rickets
B. Hyperparathyroidism (Correct Answer)
C. Skeletal dysplasia
D. Nutritional rickets

Explanation: ***Hyperparathyroidism*** - The patient exhibits **hypercalcemia** (12.8 mg/dL), **hypophosphatemia** (2.3 mg/dL), and an **elevated alkaline phosphatase** (28 KA units), which are classic hallmarks of hyperparathyroidism. - The femur fracture suggests **bone demineralization** due to chronically elevated parathyroid hormone levels, leading to increased bone turnover. Primary hyperparathyroidism is indicated by significant hypercalcemia (calcium > 11.4 mg/dL) and may lead to complications like osteoporosis [2]. *Nutritional rickets* - This condition is typically characterized by **hypocalcemia** or **normal calcium** levels, **hypophosphatemia**, and an **elevated alkaline phosphatase** due to defective bone mineralization from vitamin D deficiency [1]. - The presented case has frank **hypercalcemia**, which rules out nutritional rickets. *Renal rickets* - Also known as renal osteodystrophy, this condition primarily results in **hypocalcemia**, **hyperphosphatemia** (due to impaired phosphate excretion), and **elevated alkaline phosphatase** [1]. - The patient's **normal blood urea** and **hypercalcemia** make renal rickets unlikely. *Skeletal dysplasia* - This is a broad term for genetic disorders affecting bone and cartilage development, often leading to abnormal bone shape and fractures. - While it can cause fractures, it does not typically present with the specific constellation of **hypercalcemia** and **hypophosphatemia** seen in this patient's biochemical profile.

Question 4: What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?

A. Cinacalcet
B. Bisphosphonates
C. Calcium restriction
D. Phosphate binders (Correct Answer)

Explanation: ***Phosphate binders*** - **Phosphate binders** are the initial treatment because **hyperphosphatemia** is the primary driver of secondary hyperparathyroidism in renal disease, triggering parathyroid hormone (PTH) release [1]. - They work by binding dietary phosphate in the gastrointestinal tract, preventing its absorption and thus lowering serum phosphate levels [1]. *Cinacalcet* - **Cinacalcet** is a calcimimetic that increases the sensitivity of calcium-sensing receptors on the parathyroid gland, reducing **PTH secretion** [1]. - It is often used if **phosphate binders** and **vitamin D analogs** are insufficient in controlling PTH, making it a second-line treatment [1]. *Bisphosphonates* - **Bisphosphonates** are used to treat osteoporosis by inhibiting osteoclast activity and reducing bone resorption. - They are generally contraindicated in advanced renal osteodystrophy due to concerns about adynamic bone disease and are not an initial treatment for **secondary hyperparathyroidism**. *Calcium restriction* - While restricting dietary calcium might seem intuitive, **hypocalcemia** is often a problem in renal disease due to impaired vitamin D activation [1]. - Overly restricting calcium can worsen hypocalcemia, which would further stimulate PTH release, thus it is not an initial treatment for **secondary hyperparathyroidism**.

Question 5: A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?

A. Active 24,25 dihydroxy cholecalciferol
B. PTH (Correct Answer)
C. Serum phosphate level
D. Calcitonin

Explanation: ***PTH*** - **Parathyroid hormone (PTH)** is the primary regulator of calcium homeostasis and the key hormone that **increases in response to hypocalcemia** (low serum calcium). - In a patient on a low calcium diet for 8 weeks, **PTH secretion increases** to maintain normal serum calcium levels. - PTH acts through three main mechanisms: increasing **bone resorption** (releasing calcium from bone), enhancing renal **calcium reabsorption** in the distal tubule, and stimulating the production of **active vitamin D (1,25-dihydroxycholecalciferol)** which increases intestinal calcium absorption. *Active 24,25 dihydroxy cholecalciferol* - **24,25-dihydroxycholecalciferol** is a relatively **inactive metabolite** of vitamin D and represents a pathway of vitamin D catabolism, not activation. - The **active form** of vitamin D that increases calcium absorption is **1,25-dihydroxycholecalciferol (calcitriol)**, whose production is stimulated by PTH. - This metabolite does **not increase** in response to hypocalcemia as a compensatory mechanism. *Serum phosphate level* - A low calcium diet would **not directly lead to an increase in serum phosphate levels**. - In fact, PTH (which increases in response to low calcium) typically causes a **decrease in serum phosphate** by promoting renal phosphate excretion (phosphaturic effect). - High phosphate levels can actually exacerbate hypocalcemia by forming insoluble calcium-phosphate complexes. *Calcitonin* - **Calcitonin** is released from the thyroid parafollicular cells (C cells) in response to **high serum calcium levels** (hypercalcemia). - It acts to **lower** calcium by inhibiting osteoclast activity and reducing renal calcium reabsorption. - In hypocalcemia (low calcium diet), calcitonin secretion would **decrease, not increase**, making this the opposite of what occurs to maintain calcium homeostasis.

Question 6: A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -

A. Scurvy
B. Secondary Hyperparathyroidism (Correct Answer)
C. Vitamin D Resistant rickets
D. Primary Hyperparathyroidism

Explanation: ***Secondary Hyperparathyroidism*** - **Chronic renal failure** causes **hyperphosphatemia** and **decreased production of calcitriol (active vitamin D)**. - This leads to hypocalcemia, which stimulates the parathyroid glands to produce excessive **parathyroid hormone (PTH)**, resulting in bone demineralization and **pathological fractures** [2]. *Scurvy* - Caused by **vitamin C deficiency**, leading to impaired collagen synthesis and fragility of blood vessels. - While it can cause bone pain and potential for fractures in severe cases, it is not directly associated with **chronic renal failure** as a primary cause of pathological fracture. *Vitamin D Resistant rickets* - This is a genetic disorder (e.g., X-linked hypophosphatemia) characterized by impaired renal phosphate reabsorption and normal or elevated PTH levels. - While it causes bone demineralization, it is typically a **childhood-onset condition** [1] and not directly linked to **acquired chronic renal failure** in a 70-year-old male. *Primary Hyperparathyroidism* - Characterized by autonomous **overproduction of PTH** due to parathyroid gland adenoma or hyperplasia, leading to **hypercalcemia** and hypophosphatemia. - Unlike secondary hyperparathyroidism, which is a compensatory response to hypocalcemia in the context of renal failure, primary hyperparathyroidism is a direct parathyroid gland pathology.

Question 7: False about Marble bone disease

A. Pancytopenia
B. Associated with Type II Renal Tubular Acidosis (Correct Answer)
C. Treated with bone marrow transplantation
D. Mandible osteomyelitis

Explanation: ***Associated with Type II Renal Tubular Acidosis*** - **Marble bone disease**, or **osteopetrosis**, is characterized by increased bone density due to defective osteoclast function [1]. - It is **not typically associated** with Type II Renal Tubular Acidosis; instead, some forms of osteopetrosis, particularly carbonic anhydrase II deficiency, can lead to **Type I (distal) Renal Tubular Acidosis** [1]. *Pancytopenia* - **Osteopetrosis** leads to bone marrow encroachment, reducing the space available for hematopoiesis. - This often results in **pancytopenia** (anemia, leukopenia, and thrombocytopenia) due to bone marrow failure. *Treated with bone marrow transplantation* - **Bone marrow transplantation (BMT)** is a crucial treatment for severe forms of osteopetrosis, especially the infantile malignant autosomal recessive type. - BMT can introduce functional **osteoclast precursors** from the donor, which can then differentiate and restore bone resorption. *Mandible osteomyelitis* - Patients with **osteopetrosis** have bones that are dense but paradoxically brittle, making them prone to fractures and infections. - The **mandible** is particularly susceptible to **osteomyelitis** due to its dense structure and vascular compromise in osteopetrosis, often complicated by dental issues.

Question 8: Marble bone disease is:

A. Osteosclerosis
B. Histiocytosis X
C. Osteopetrosis (Correct Answer)
D. Osteomalacia

Explanation: ***Osteopetrosis*** - **Osteopetrosis**, also known as **marble bone disease**, is a rare genetic disorder characterized by abnormally dense bones due to a defect in **osteoclast function** [1]. - Impaired bone resorption leads to an accumulation of woven bone, causing bones to be fragile despite their density [1]. *Osteosclerosis* - **Osteosclerosis** is a general term for increased bone density and can be a feature of various conditions, including osteopetrosis. - However, it is a descriptive term rather than a specific disease diagnosis equivalent to marble bone disease. *Histiocytosis X* - **Histiocytosis X**, also known as **Langerhans cell histiocytosis**, is a rare disorder involving the proliferation of Langerhans cells. - It primarily affects bone but can also involve other organs, presenting with lytic lesions rather than increased bone density. *Osteomalacia* - **Osteomalacia** is a condition characterized by inadequate mineralization of bone tissue, leading to soft and weakened bones. - It is typically caused by **vitamin D deficiency** and is the opposite of increased bone density. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1188-1189.

Question 9: The following gait is seen due to weakness of:

A. Gluteus maximus
B. Gluteus medius (Correct Answer)
C. Psoas major
D. Tibialis anterior

Explanation: ***Gluteus medius*** - Weakness of the **gluteus medius** leads to a **Trendelenburg gait**, where the pelvis drops on the unsupported side during the swing phase of gait. - The image suggests pelvic tilting, which is characteristic of the body attempting to compensate for the inability of the gluteus medius to stabilize the pelvis. *Gluteus maximus* - Weakness of the gluteus maximus causes difficulty in **hip extension**, resulting in a **lurching gait** where the trunk is thrown backward at heel strike. - This is commonly known as a **gluteus maximus lurch**, which is not depicted in an obvious manner here. *Psoas major* - Weakness of the psoas major would primarily affect **hip flexion**, making it difficult to lift the leg off the ground (e.g., during the swing phase). - This would result in compensatory movements such as circumduction or hiking the hip, rather than the characteristic pelvic drop. *Tibialis anterior* - Weakness of the tibialis anterior causes **foot drop**, leading to a **steppage gait** where the knee is lifted high to avoid dragging the foot. - The image does not show a foot drop or high stepping, thus ruling out tibialis anterior weakness.

Question 10: The commonest complication of fracture of clavicle is :

A. non union
B. avascular necrosis
C. Neurovascular injury
D. malunion (Correct Answer)

Explanation: ***malunion*** - **Malunion** is the most frequent complication following a clavicle fracture, meaning the bone heals in an anatomically incorrect or deformed position. - This often results in a palpable bump or cosmetic deformity, and can occasionally cause functional impairment. *non union* - **Non-union** occurs when the fracture fails to heal completely, leaving a persistent gap between the bone fragments. - While possible, it is less common than malunion in clavicle fractures, especially with appropriate management. *avascular necrosis* - **Avascular necrosis** is rare in clavicle fractures because the clavicle has a rich blood supply. - It typically affects bones with precarious blood supply, such as the femoral head or scaphoid. *Neurovascular injury* - **Neurovascular injury** involving the subclavian vessels or brachial plexus is a serious but relatively rare complication of clavicle fractures. - While possible, especially with displaced fractures, it is not the most common adverse outcome.

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