Diabetes Mellitus in Children — MCQs
Retinopathy is most likely to be seen with which of the following conditions?
Which of the following is NOT a feature of Autoimmune Polyglandular Syndrome type 1 (APS-1)?
A 14-year-old male presents with type I diabetes mellitus. His mother wants to know if the boy's brother might also have an increased risk of getting the disease. Which of the following genotypes, if present in the brother, would be associated with the greatest risk of developing diabetes?
In a comatose patient with a blood glucose level of 750 mg/dL, which test is most important to perform in addition to serum potassium?
A patient with DKA has a pH of 7.1, Na 130, and K 5.5. What is the best initial treatment?
In a newly diagnosed case of a sick child with type 1 diabetes mellitus (DM), insulin was given. Which of the following will increase:
A 3.8 kg baby of a diabetic mother developed seizures 32 hours after birth. The most probable cause would be?
A diabetic patient's fasting blood glucose level is found to be $160 \mathrm{mg} / \mathrm{dL}$. What will you advise the patient regarding non-pharmacological management?
In a 2-5 year-old child with DM, target HbA1C is:
Screening for nephropathy in prepubertal children with type 1 DM should be initiated after how many years of disease onset?
Diabetes Mellitus in Children Indian Medical PG Practice Questions and MCQs
Question 1: Retinopathy is most likely to be seen with which of the following conditions?
- A. Gestational diabetes
- B. Juvenile diabetes started before puberty
- C. Type 2 diabetes of 8 years duration (Correct Answer)
- D. Type 1 diabetes of 5 years duration
Explanation: **Type 2 diabetes of 8 years duration** - **Diabetic retinopathy** is a common microvascular complication of diabetes mellitus [1]. - The risk of retinopathy increases with the **duration of diabetes** and the **severity of hyperglycemia**, making an 8-year duration with type 2 diabetes a significant risk factor [1]. *Type 1 diabetes of 5 years duration* - While type 1 diabetes can cause retinopathy, a 5-year duration is generally considered relatively short for the development of significant retinopathy, especially in early stages. - The risk of retinopathy in **Type 1 diabetes** becomes more pronounced after 10-15 years, though it can occur earlier. *Gestational diabetes* - **Gestational diabetes** is a temporary condition occurring during pregnancy and does not typically lead to chronic complications like retinopathy. - Retinopathy is rare in gestational diabetes because the disease duration is short and usually resolves post-partum. *Juvenile diabetes started before puberty* - **Juvenile diabetes** is synonymous with Type 1 diabetes [2]. Although early onset of diabetes increases lifetime risk, the duration of diabetes is a more critical factor for retinopathy development. - Without a specified duration, it's less predictive than an established longer duration of Type 2 diabetes.
Question 2: Which of the following is NOT a feature of Autoimmune Polyglandular Syndrome type 1 (APS-1)?
- A. Mucocutaneous candidiasis
- B. Addison's disease
- C. Hypoparathyroidism
- D. Autoimmune thyroiditis (Correct Answer)
Explanation: ### 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.
Question 3: A 14-year-old male presents with type I diabetes mellitus. His mother wants to know if the boy's brother might also have an increased risk of getting the disease. Which of the following genotypes, if present in the brother, would be associated with the greatest risk of developing diabetes?
- A. DR2/DR4
- B. DR3/DR4 (Correct Answer)
- C. DR2/DR2
- D. B27/B27
Explanation: ***DR3/DR4*** - The combination of **HLA-DR3** and **HLA-DR4** is the strongest genetic risk factor for **Type 1 diabetes mellitus (T1DM)**, particularly in individuals of European descent. - These alleles are associated with increased susceptibility to autoimmune destruction of pancreatic beta cells [1]. *DR2/DR4* - While **DR4** is a risk allele for Type 1 diabetes, **DR2 (specifically DRB1*1501)** is generally considered to be protective against the disease. - The presence of the protective DR2 allele would likely mitigate the increased risk conferred by DR4. *DR2/DR2* - **HLA-DR2 (DRB1*1501)** is largely recognized as a protective allele against **Type 1 diabetes**, meaning individuals with this genotype have a lower risk of developing the disease [1]. - Its presence is associated with a reduced susceptibility to autoimmune conditions like T1DM. *B27/B27* - **HLA-B27** is primarily associated with **seronegative spondyloarthropathies** such as ankylosing spondylitis and reactive arthritis, and not directly with an increased risk of Type 1 diabetes mellitus. - This allele is involved in different autoimmune pathways than those implicated in T1DM.
Question 4: In a comatose patient with a blood glucose level of 750 mg/dL, which test is most important to perform in addition to serum potassium?
- A. Serum creatinine
- B. Serum sodium
- C. Serum ketones
- D. Arterial blood gases (Correct Answer)
Explanation: ***Arterial blood gases*** - In a comatose patient with severe hyperglycemia (750 mg/dL), **arterial blood gases (ABGs)** are crucial to assess for **acidosis**, which could indicate **diabetic ketoacidosis (DKA)** or **hyperosmolar hyperglycemic state (HHS)** with lactic acidosis [1], [4]. - The **pH**, **bicarbonate (HCO3-)**, and **pCO2** levels from ABGs help determine the severity and type of metabolic derangement, guiding immediate treatment, especially for potential **cerebral edema** [3], [4]. *Serum creatinine* - While important for assessing **kidney function** in hyperosmolar states, it does not directly evaluate the immediate acid-base status that is critical for neurologic function in a comatose patient. - Renal insufficiency can exacerbate electrolyte imbalances and fluid overload but is secondary to the immediate need for acid-base assessment. *Serum sodium* - **Serum sodium** is important for calculating **effective serum osmolality**, which is elevated in both DKA and HHS, contributing to mental status changes [2]. - However, while important, it does not provide information about the **acid-base balance**, which is a more critical determinant of immediate neurologic stability and treatment in deep coma. *Serum ketones* - **Serum ketones** are essential for distinguishing between **DKA** (high ketones) and **HHS** (low or absent ketones) [4]. - While vital for diagnosis, ketones alone do not give the full picture of **acid-base status** (pH, bicarbonate) which is directly assessed by ABGs and more immediately actionable in managing a severely ill, comatose patient [1].
Question 5: A patient with DKA has a pH of 7.1, Na 130, and K 5.5. What is the best initial treatment?
- A. IV insulin
- B. IV fluids (Correct Answer)
- C. IV potassium
- D. IV bicarbonate
Explanation: ***IV fluids*** - Initial management of **diabetic ketoacidosis (DKA)** prioritizes aggressive **intravenous fluid resuscitation** to correct dehydration and improve renal perfusion, thereby facilitating ketone and glucose excretion [1]. - This step is critical before insulin administration to prevent rapid drops in osmolality, which can lead to **cerebral edema** [2]. *IV insulin* - While critical for resolving DKA by stopping ketone production and lowering glucose, **insulin is typically started after initial fluid resuscitation** and only once potassium levels are stable or >3.3 mEq/L to prevent hypokalemia. - Early insulin without adequate fluid replacement can worsen dehydration and increase the risk of **cerebral edema**. *IV potassium* - Although DKA patients are typically **potassium-depleted**, despite what appears to be normal or high serum potassium due to extracellular shift, IV potassium replacement is usually initiated only once serum potassium falls below 5.3 mEq/L and after the start of insulin, which drives potassium into cells [1]. - Administering potassium too early without baseline potassium re-evaluation after initial fluid resuscitation could lead to **hyperkalemia** if the initial high level is truly representative. *IV bicarbonate* - Bicarbonate therapy for DKA is controversial and generally **not recommended** unless the pH is extremely low, typically < 6.9, or in cases of severe cardiovascular instability. - Rapid correction of acidosis can lead to **cerebral edema**, **rebound metabolic alkalosis**, paradoxical central nervous system acidosis, and worsening hypokalemia.
Question 6: In a newly diagnosed case of a sick child with type 1 diabetes mellitus (DM), insulin was given. Which of the following will increase:
- A. Breathing rate
- B. Urine osmolality
- C. Glucosuria
- D. pH (Correct Answer)
Explanation: ***pH*** - In newly diagnosed, uncontrolled **Type 1 DM**, patients often present with **diabetic ketoacidosis (DKA)**, leading to metabolic acidosis and a **critically low pH** (typically <7.3). - Administering insulin corrects the underlying metabolic derangements, reducing **ketoacid production** and allowing the body's **buffer systems** to restore pH towards normal. - **Correction of acidosis** is the **primary therapeutic goal** and the most clinically significant parameter that increases with insulin therapy in DKA. *Breathing rate* - In **DKA**, patients often exhibit **Kussmaul respirations** (deep, rapid breathing) as a compensatory mechanism to blow off CO2 and reduce acidosis. - As insulin therapy corrects the acidosis, the need for this compensatory mechanism decreases, leading to a **reduction**, not an increase, in breathing rate. *Urine osmolality* - In uncontrolled **Type 1 DM** and **DKA**, high blood glucose leads to **osmotic diuresis**, where glucose pulls water into the urine, resulting in polyuria and typically **low urine osmolality** (dilute urine). - While insulin therapy may allow some increase in urine concentration as osmotic diuresis decreases, this is a **secondary effect** and not the primary clinical focus in acute DKA management. - Additionally, initial fluid resuscitation in DKA treatment maintains diuresis, so urine osmolality changes are variable and less predictable. *Glucosuria* - **Glucosuria** (glucose in the urine) is a hallmark of uncontrolled diabetes due to hyperglycemia exceeding the renal threshold for glucose reabsorption. - Insulin treatment lowers blood glucose levels, which in turn **reduces or eliminates glucosuria**, as the kidneys no longer filter excessive amounts of glucose.
Question 7: A 3.8 kg baby of a diabetic mother developed seizures 32 hours after birth. The most probable cause would be?
- A. Hypoglycemia
- B. Hypocalcemia (Correct Answer)
- C. Birth asphyxia
- D. Intraventricular hemorrhage
Explanation: ***Hypocalcemia*** - In infants of diabetic mothers (IDM), hypocalcemia typically presents at **24-72 hours of life**, making it the most probable cause of seizures at 32 hours. - The mechanism involves **functional hypoparathyroidism** secondary to maternal hyperparathyroidism and **hypomagnesemia**, which impairs parathyroid hormone secretion and action. - IDMs have increased metabolic demands and altered calcium homeostasis due to intrauterine metabolic disturbances. - **Timing is key**: The presentation at 32 hours strongly favors hypocalcemia over hypoglycemia in the differential diagnosis. *Hypoglycemia* - While hypoglycemia is indeed common in IDMs due to **fetal hyperinsulinemia**, it typically occurs much earlier—within the **first 2-24 hours of life** (peak at 1-3 hours). - By 32 hours, hypoglycemia would usually have been detected through routine monitoring or would have manifested earlier with symptoms. - Neonatal hypoglycemia causes seizures, but the **timing in this case makes it less likely** than hypocalcemia. *Birth asphyxia* - Birth asphyxia leads to hypoxic-ischemic encephalopathy with seizures typically presenting within the **first 12-24 hours**. - Would be accompanied by other neurological signs like hypotonia, altered consciousness, and poor feeding from birth. - No history suggesting birth complications is provided in the scenario. *Intraventricular hemorrhage* - IVH is primarily a complication of **prematurity**, particularly in very low birth weight infants. - This 3.8 kg baby is likely term or large-for-gestational-age, making IVH uncommon unless significant birth trauma occurred. - IVH presents with acute neurological deterioration, bulging fontanelle, and altered consciousness—not mentioned here.
Question 8: A diabetic patient's fasting blood glucose level is found to be $160 \mathrm{mg} / \mathrm{dL}$. What will you advise the patient regarding non-pharmacological management?
- A. At least 25-35 g of dietary fibre
- B. <30 % of the calories should come from fat (Correct Answer)
- C. Dietary cholesterol <300 mg per day
- D. <2.3 g sodium intake every day
Explanation: ***<30 % of the calories should come from fat*** - Reducing dietary fat intake to less than 30% of total calories is a crucial non-pharmacological strategy for diabetic patients to manage blood glucose levels and prevent cardiovascular complications [1]. - Excess dietary fat, especially saturated and trans fats, can contribute to insulin resistance and weight gain, both of which negatively impact glycemic control [1]. *At least 25-35 g of dietary fibre* - While adequate dietary fiber (typically 25-30g for adults, sometimes up to 35g for men) is beneficial for managing blood glucose, it is generally recommended as a baseline for healthy eating and not the primary or most impactful intervention to address a fasting glucose of 160 mg/dL [1]. - Fiber helps slow glucose absorption and can improve insulin sensitivity, but a specific "at least 25-35g" statement without further context on total caloric intake or other macronutrient distribution might not be the most targeted advice for this specific glucose level [1]. *Dietary cholesterol <300 mg per day* - Limiting dietary cholesterol to less than 300 mg per day is a general recommendation for cardiovascular health, which is particularly important for diabetic patients due to their increased risk of atherosclerosis [2]. - However, for directly addressing a fasting blood glucose of 160 mg/dL, focusing on overall fat intake and carbohydrate quality would have a more immediate impact on glucose control than dietary cholesterol alone. *<2.3 g sodium intake every day* - Restricting sodium intake to less than 2.3 g per day is recommended for managing hypertension and reducing cardiovascular risk, which is often comorbid with diabetes [2]. - While important for overall health in diabetic patients, this recommendation does not directly target blood glucose control and would not be the primary non-pharmacological advice for a fasting glucose of 160 mg/dL.
Question 9: In a 2-5 year-old child with DM, target HbA1C is:
- A. < 8% (Correct Answer)
- B. < 7%
- C. < 7.5%
- D. < 6.5%
Explanation: ***< 8%*** - For children aged **2-5 years** with diabetes mellitus, the target **HbA1c** is **< 8%** (some guidelines recommend < 8.5%) to balance glycemic control with the significant risk of hypoglycemia. - This age group is at **critical neurodevelopmental stage**, and severe hypoglycemia can have lasting cognitive effects, hence a more lenient target is recommended. - The higher target accounts for **unpredictable eating patterns, variable activity levels**, and difficulty in recognizing hypoglycemic symptoms at this young age. *< 7%* - An **HbA1c** target of **< 7%** is too stringent for very young children (2-5 years) and significantly increases the risk of **severe hypoglycemia**. - This target may be appropriate for **adults** or older adolescents with good awareness and self-management skills, but not for this vulnerable age group. - Achieving this target in toddlers would require intensive monitoring and could compromise safety and quality of life. *< 7.5%* - An **HbA1c** target of **< 7.5%** is the recommended target for **older children (6-12 years)** and **adolescents (13-19 years)**, not for children aged 2-5 years. - While more achievable than < 7%, this target is still too aggressive for the 2-5 year age group and increases hypoglycemia risk without proportional long-term benefit. *< 6.5%* - An **HbA1c** target of **< 6.5%** is far too aggressive for children aged 2-5 years and would pose an **unacceptable risk of severe and frequent hypoglycemia**. - This target approaches near-normal glycemia and is only considered in select adult patients who can achieve it safely with minimal hypoglycemia risk. - In young children, such tight control could result in seizures, developmental harm, and psychological stress for families.
Question 10: Screening for nephropathy in prepubertal children with type 1 DM should be initiated after how many years of disease onset?
- A. 3 years
- B. 4 years
- C. 2 years
- D. 5 years (Correct Answer)
Explanation: ***5 years*** - The **American Diabetes Association (ADA)** recommends initiating screening for **diabetic nephropathy** in type 1 DM patients starting at **5 years after diagnosis**, provided the patient has reached **puberty (Tanner stage 2-3) or age ≥11 years**. - In prepubertal children, even with 5+ years of disease duration, screening is typically **deferred until puberty** because microvascular complications are exceedingly rare before pubertal onset. - The **5-year duration threshold** is the standard timeframe, but it is coupled with pubertal status as a key criterion. *3 years* - This duration is too early according to current **ADA guidelines**, which recommend screening after **5 years** of disease duration. - The risk of **nephropathy** developing within 3 years in type 1 DM patients, especially prepubertal children, is very low. *4 years* - While closer to the guideline, **4 years** is still premature compared to the evidence-based **5-year threshold** recommended by major diabetes organizations. - Early screening before 5 years would increase false positives and unnecessary interventions. *2 years* - Initiating screening after only **2 years** is far too early and not supported by current evidence. - **Microvascular complications** including nephropathy require longer disease duration to develop, making 2-year screening inefficient and not cost-effective.
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