Endocrinology Practice Questions

Q: Which of the following clinical findings is characteristic of both osteomalacia and rickets?

muscle weakness. ***Muscle weakness*** - **Muscle weakness** is a common symptom in both rickets (in children) and osteomalacia (in adults) due to **impaired mineralization of bone matrix** and compromised muscle function [1]. - This weakness often presents as **difficulty walking**, standing, or performing daily activities. *Frontal bossing in the skull* - **Frontal bossing** (prominent forehead) is a specific sign of **rickets** in children, resulting from excessive unmineralized osteoid on the skull [1]. - It is not typically seen in adult **osteomalacia**, as the skull bones are already formed. *Defects in tooth enamel* - **Defects in tooth enamel** are primarily associated with a prolonged and severe deficiency of **vitamin D or calcium during tooth development**, which is characteristic of childhood **rickets**. - While vitamin D and calcium are crucial for overall bone health, enamel defects are less common or severe in adult-onset **osteomalacia**. *Prominent costochondral junctions* - **Prominent costochondral junctions** (rachitic rosary) are a classic sign of **rickets** in children, caused by the enlargement of the cartilage at the ends of the ribs due to defective mineralization [1]. - This finding is specific to growing children and is not observed in adults with **osteomalacia**.

Q: Minimum fasting BGL for diagnosis of diabetes mellitus is:

126 mg/dl. ***126 mg/dl*** - A **fasting plasma glucose (FPG)** of **126 mg/dL (7.0 mmol/L)** or higher is diagnostic of diabetes mellitus. - This value indicates sustained hyperglycemia that meets the criteria set by major health organizations. *114 mg/dl* - An FPG of **114 mg/dL** falls within the range for **prediabetes** (100-125 mg/dL) or impaired fasting glucose, not diabetes. - While it indicates a higher risk for developing diabetes, it does not meet the diagnostic threshold for the disease itself. *120 mg/dl* - An FPG of **120 mg/dL** is also considered **prediabetes** or impaired fasting glucose, as it is below the diagnostic threshold for diabetes. - Patients in this range should monitor their glucose levels and adopt lifestyle changes to prevent progression to diabetes. *132 mg/dl* - While **132 mg/dL** certainly indicates diabetes, the question asks for the **minimum** fasting BGL for diagnosis. - The threshold of **126 mg/dL** is the widely accepted minimum diagnostic value.

Q: What is normal range of glycosylated haemoglobin (HbA1c) for adequate glycaemic control in diabetic patient-

4 % to 6 %. ***4% to 6%*** - This range represents **excellent glycemic control** and is closest to the recommended target of **less than 7%** for adequate diabetes management [1]. - While it requires careful monitoring for **hypoglycemia risk**, it significantly reduces the risk of **microvascular** and **macrovascular complications** [1]. *10% to 12%* - This range indicates very **poor glycemic control** and significantly increases the risk of both acute and chronic diabetes complications. - An HbA1c in this range suggests that the patient's blood glucose levels have been consistently high over several months. *8% to 10%* - While better than 10-12%, an HbA1c in this range still indicates **suboptimal glycemic control** for most diabetic patients. - It suggests a need for adjustments in treatment, diet, or lifestyle to prevent long-term complications. *6% to 8%* - This range is **too broad** for adequate glycemic control, with the upper limit of 8% being acceptable only for **elderly patients** or those with **significant comorbidities** [1]. - For most diabetic patients seeking adequate control, this range exceeds the recommended target of **less than 7%** [1].

Q: Sirtuin is associated with?

All of the options. ***All of the options*** - **Sirtuins** are a family of protein deacetylases and ADP-ribosyltransferases that play crucial roles in regulating various cellular processes, including **metabolism**, gene expression, and DNA repair. - Their involvement in these fundamental processes links them to the pathogenesis and progression of **diabetes**, **aging-related diseases**, and **cancer**. *Diabetes* - Sirtuins, particularly **SIRT1**, influence **insulin sensitivity** and glucose metabolism. - Dysregulation of sirtuin activity has been implicated in the development and progression of **type 2 diabetes**. *Aging* - Sirtuins are often referred to as **"longevity genes"** due to their role in regulating cellular responses to stress and extending lifespan in various organisms. - They are involved in pathways that maintain cellular integrity and function, thereby impacting the **aging process**. *Cancer* - The role of sirtuins in **cancer** is complex and can be either tumor-suppressive or oncogenic depending on the specific sirtuin, cancer type, and cellular context. - They regulate pathways involved in **cell proliferation**, apoptosis, and DNA repair, making them potential targets for cancer therapy.

Q: Hypertension with androgenization of a female child is a feature of congenital adrenal hyperplasia due to deficiency of:

C-11 hydroxylase. ***C-11 hydroxylase*** - Deficiency of **C-11 hydroxylase** leads to accumulation of 11-deoxycorticosterone (DOC) and 11-deoxycortisol [1]. - **DOC** has mineralocorticoid activity, causing **hypertension**, while the shunting of precursors to the adrenal androgen pathway results in **androgenization** [1]. *C-17 hydroxylase* - **C-17 hydroxylase deficiency** results in decreased sex steroids and cortisol, leading to hypertension due to increased mineralocorticoids [1]. - However, the lack of androgens would cause **undervirilization** in males and **lack of secondary sexual characteristics** in females, rather than androgenization. *C-21 hydroxylase* - **C-21 hydroxylase deficiency** is the most common cause of congenital adrenal hyperplasia [1]. - It leads to **androgenization** but typically causes **hypotension** and **salt-wasting** due to deficient mineralocorticoid production, not hypertension. *Desmolase* - **Desmolase (P450scc) deficiency** is a very severe form of congenital adrenal hyperplasia, impairing the synthesis of all adrenal steroids [1]. - This would lead to severe **adrenal insufficiency**, **hypotension**, and **salt-wasting**, with a lack of androgenization due to impaired sex steroid synthesis [1].

Q: Which of the following is NOT a feature of Autoimmune Polyglandular Syndrome type 1 (APS-1)?

Autoimmune thyroiditis. ### Autoimmune thyroiditis - **Autoimmune thyroiditis** is a key component of **Autoimmune Polyglandular Syndrome type 2 (APS-2)**, not APS-1 [1]. - APS-1 is distinguished by its classic triad, which does not include autoimmune thyroiditis as a primary feature [1]. ### Mucocutaneous candidiasis - **Chronic mucocutaneous candidiasis** is a defining feature of APS-1, affecting nearly all patients [1]. - This fungal infection is often the **first symptom** to appear in patients with APS-1. ### Addison's disease - **Addison's disease (primary adrenal insufficiency)** is a highly prevalent component of APS-1, occurring in over 80% of patients [1]. - It results from the autoimmune destruction of the adrenal cortex. ### Hypoparathyroidism - **Hypoparathyroidism** is a crucial diagnostic criterion for APS-1, occurring in over 70% of affected individuals [1]. - It leads to **hypocalcemia** due to inadequate parathyroid hormone production.

Q: All are causes of Osteoporosis, except:

Hypothyroidism. Hypothyroidism - **Hypothyroidism** is generally associated with decreased bone turnover and can lead to **increased bone mineral density**, rather than osteoporosis. - In some cases, severe hypothyroidism might cause secondary osteoporosis due to associated **vitamin D deficiency** or other factors, but it is not a direct cause. Thyrotoxicosis - **Thyrotoxicosis** (hyperthyroidism) accelerates **bone remodeling**, leading to increased **bone resorption** and a net loss of bone mass. - This increases the risk of osteoporosis and fractures due to the catabolic effects of excess **thyroid hormone**. Old age - **Old age** is a major risk factor for osteoporosis due to a natural decline in **bone mineral density** and bone formation over time [2]. - Hormonal changes, such as **estrogen deficiency** in postmenopausal women and reduced **testosterone** in men [1], contribute significantly to age-related bone loss [2]. Chronic heparin therapy - **Chronic heparin therapy** (especially **unfractionated heparin**) can cause osteoporosis due to its effects on **osteoblast activity** and **collagen synthesis**. - It interferes with **bone formation** and can enhance **bone resorption**, leading to a decrease in bone density.

Q: Patchy hair loss with hyperhidrosis of skin points to the diagnosis of -

Hyperthyroidism. ***Hyperthyroidism*** - **Hyperthyroidism** can cause **diffuse hair thinning** or **patchy hair loss**, and increased **sweating (hyperhidrosis)** is a classic symptom due to increased metabolic rate [1]. - Other common symptoms include **heat intolerance**, **tachycardia**, **weight loss**, and **tremors**. *Alopecia areata* - Characterized by **well-demarcated, smooth non-scarring patches of hair loss**, often with **exclamation mark hairs** [1]. - It is an **autoimmune condition** and typically does not present with hyperhidrosis as a primary symptom. *Trichotillomania* - Defined by the **compulsive pulling out of one's hair**, leading to **irregular patches of hair loss** with hairs of varying lengths [1]. - It is a **psychiatric disorder** and does not cause hyperhidrosis. *Adenoma sebaceum* - This term is a misnomer for **facial angiofibromas**, which are small, red-to-flesh-colored papules typically found on the nose and cheeks. - These lesions are a common feature of **Tuberous Sclerosis Complex** and do not cause hair loss or hyperhidrosis.

Q: Apparent mineralocorticoid excess is due to

11-β hydroxysteroid dehydrogenase. ***11-β hydroxysteroid dehydrogenase*** - Apparent mineralocorticoid excess (AME) is caused by a deficiency of **11-β-hydroxysteroid dehydrogenase type 2 (11β-HSD2)**, which is responsible for inactivating **cortisol** to **cortisone** [1]. - Without proper inactivation, elevated cortisol levels can then **bind to and activate mineralocorticoid receptors (MR)** in the kidney, leading to symptoms mimicking hyperaldosteronism [1]. *Sgk gene* - The **SGK1 gene** encodes for **serum and glucocorticoid-regulated kinase 1**, which plays a role in renal sodium absorption, but not directly in the cause of AME [1]. - While **SGK1** is involved in epithelial sodium channel (ENaC) regulation, its overactivity is a downstream effect, not the primary cause of AME [1]. *CYP 11B2* - **CYP11B2** (aldosterone synthase) is responsible for the final step in **aldosterone synthesis** [1]. - While it's crucial for mineralocorticoid production, a deficiency in **11β-HSD2** causes **cortisol-induced mineralocorticoid effects**, not issues with aldosterone synthesis itself. *CYP11A* - **CYP11A** (cholesterol side-chain cleavage enzyme) initiates the synthesis of all steroid hormones from **cholesterol** [1]. - Defects in **CYP11A** would lead to a more severe and broad deficiency in steroid production, not specifically apparent mineralocorticoid excess.

Question 1

Which of the following clinical findings is characteristic of both osteomalacia and rickets?

Accepted Answer

muscle weakness

Answer

frontal bossing in the skull

Answer

defects in tooth enamel

Answer

prominent costochondral junctions

Question 2

Minimum fasting BGL for diagnosis of diabetes mellitus is:

Accepted Answer

126 mg/dl

Answer

114 mg/dl

Answer

120 mg/dl

Answer

132 mg/dl

Question 3

What is normal range of glycosylated haemoglobin (HbA1c) for adequate glycaemic control in diabetic patient-

Accepted Answer

4 % to 6 %

Answer

10 % to 12 %

Answer

8 % to 10 %

Answer

6% to 8 %

Question 4

Sirtuin is associated with?

Accepted Answer

All of the options

Answer

Diabetes

Answer

Aging

Answer

Cancer

Question 5

Hypertension with androgenization of a female child is a feature of congenital adrenal hyperplasia due to deficiency of:

Accepted Answer

C-11 hydroxylase

Answer

C-17 hydroxylase

Answer

C-21 hydroxylase

Answer

Desmolase

Question 6

Which of the following is NOT a feature of Autoimmune Polyglandular Syndrome type 1 (APS-1)?

Accepted Answer

Autoimmune thyroiditis

Answer

Mucocutaneous candidiasis

Answer

Addison's disease

Answer

Hypoparathyroidism

Question 7

The most common presentation of hyperparathyroidism beyond the neonatal period is –

Accepted Answer

Stones, bones, abdominal groans, thrones and psychiatric overtones

Answer

Bronchospasm

Answer

Seizure

Answer

Syncope secondary to prolonged QT intervals

Question 8

All are causes of Osteoporosis, except:

Accepted Answer

Hypothyroidism

Answer

Thyrotoxicosis

Answer

Old age

Answer

Chronic heparin therapy

Question 9

Patchy hair loss with hyperhidrosis of skin points to the diagnosis of -

Accepted Answer

Hyperthyroidism

Answer

Alopecia areata

Answer

Trichotillomania

Answer

Adenoma sebaceum

Question 10

Apparent mineralocorticoid excess is due to

Accepted Answer

11-β hydroxysteroid dehydrogenase

Answer

Sgk gene

Answer

CYP 11B2

Answer

CYP11A

Endocrinology — MCQs

Endocrinology — MCQs

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