Endocrine Emergencies — MCQs
Which of the following is a classic feature of pheochromocytoma?
A patient with DKA has a pH of 7.1, Na 130, and K 5.5. What is the best initial treatment?
Thyroid storm during surgery is due to?
In a patient presenting with diabetic ketoacidosis (DKA), what is the most appropriate immediate treatment?
Which of the following conditions is most commonly associated with neonatal hypoglycemia?
Insulin of choice for the treatment of diabetic ketoacidosis is:
A 28 year female presented to emergency with fever, agitation and delirium. She was on regular medication of Carbimazole 40 mg daily, but missed her doses for the last 2 days. Which of the following scoring systems would you like to do to assess severity of disease?
What is the primary effect of beta blockers in the management of thyroid storm?
A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -
Which of the following statements about pheochromocytoma is true?
Endocrine Emergencies Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is a classic feature of pheochromocytoma?
- A. Headache (Correct Answer)
- B. Hyperkalemia
- C. Bradycardia
- D. Hypoglycemia
Explanation: ***Headache*** - Severe, pounding **headaches** are a classic symptom due to the paroxysmal release of **catecholamines** causing extreme hypertension. - This symptom is often one of the "P's" associated with pheochromocytoma: palpitations, perspiration, pallor, and paroxysmal hypertension. *Hyperkalemia* - **Hyperkalemia** is not typically associated with pheochromocytoma; rather, the excessive catecholamine release can sometimes cause stress-induced hypokalemia due to increased intracellular potassium shift. - The primary electrolyte imbalance to watch for is related to severe hypertension complications. *Bradycardia* - **Bradycardia** is generally not a feature of pheochromocytoma; instead, patients frequently experience **tachycardia** and **palpitations** due to the stimulatory effects of catecholamines on the heart. - The sympathetic nervous system activation leads to an increased heart rate. *Hypoglycemia* - **Hypoglycemia** is uncommon in pheochromocytoma; the excess catecholamines typically lead to **hyperglycemia** by promoting glycogenolysis and gluconeogenesis, and inhibiting insulin release. - This elevation in blood sugar can mimic diabetes, sometimes requiring insulin therapy.
Question 2: 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 3: Thyroid storm during surgery is due to?
- A. Perioperative intervention
- B. Inadequate preoperative preparation (Correct Answer)
- C. Glucocorticoid side effect
- D. Rough handling during surgery
Explanation: ***Inadequate preoperative preparation*** - **Thyroid storm** is a life-threatening exaggeration of hyperthyroidism, often triggered in patients who are **inadequately prepared** for surgery. - This typically means insufficient control of thyroid hormone levels (e.g., with antithyroid drugs, beta-blockers) prior to a surgical stressor. *Perioperative intervention* - While surgery itself is a stressor, a properly performed **perioperative intervention** on a well-prepared patient is less likely to trigger thyroid storm. - The problem is not the intervention itself, but the patient's underlying uncontrolled hyperthyroid state. *Glucocorticoid side effect* - **Glucocorticoids** are often used to treat thyroid storm, not cause it. - They help reduce peripheral conversion of T4 to T3 and provide adrenal support. *Rough handling during surgery* - While **rough handling** during thyroid surgery (e.g., excessive manipulation of the thyroid gland) can, in theory, release some thyroid hormone, it is a less significant factor in triggering thyroid storm than overall systemic hyperthyroidism. - The primary cause remains **inadequate systemic control** of thyroid hormone levels.
Question 4: In a patient presenting with diabetic ketoacidosis (DKA), what is the most appropriate immediate treatment?
- A. Administration of an oral hypoglycemic agent
- B. Administration of bicarbonate
- C. Administration of insulin (Correct Answer)
- D. Close observation only
Explanation: ***Administration of insulin*** - **Insulin therapy** is critical in DKA to reverse the underlying metabolic abnormalities by stopping ketogenesis and facilitating glucose uptake into cells [1]. - It is typically administered intravenously at a continuous rate, after initial **fluid resuscitation**, to gradually lower blood glucose and resolve acidosis [1]. *Administration of an oral hypoglycemic agent* - **Oral hypoglycemic agents** are ineffective in DKA because these patients typically have an absolute or relative **insulin deficiency** and **profound insulin resistance** due to stress hormones [3]. - Moreover, they are not suitable for acutely ill patients who may have impaired gastrointestinal absorption. *Administration of bicarbonate* - **Bicarbonate administration** is generally not recommended in DKA unless the **pH is extremely low** (e.g., < 6.9 or 7.0) due to potential risks like paradoxical central nervous system acidosis and fluid overload. - The acidosis usually resolves with **insulin therapy** and **fluid resuscitation** as ketone body production ceases and they are metabolized [1]. *Close observation only* - **Diabetic ketoacidosis** is a medical emergency requiring urgent and aggressive intervention, not just observation [2]. - Delaying treatment can lead to severe complications, including **cerebral edema**, **coma**, and **death** [2].
Question 5: Which of the following conditions is most commonly associated with neonatal hypoglycemia?
- A. Infants born to diabetic mothers (Correct Answer)
- B. Infants with low birth weight
- C. Infants born to mothers with toxaemia of pregnancy
- D. Premature infants
Explanation: ***Infants born to diabetic mothers*** - Maternal hyperglycemia leads to fetal **hyperinsulinism**, which continues after birth when the glucose supply from the mother is interrupted. - This persistent hyperinsulinism rapidly consumes the available glucose in the neonate, leading to profound and often symptomatic **hypoglycemia**. - This is the **most common** association with neonatal hypoglycemia encountered in clinical practice. *Infants with low birth weight* - While **low birth weight (LBW)** infants are at increased risk for hypoglycemia due to limited glycogen stores and impaired gluconeogenesis, it is not the most common association compared to infants of diabetic mothers. - Their hypoglycemia tends to be due to limited metabolic reserves, whereas in infants of diabetic mothers, it's driven by **insulin excess**. *Infants born to mothers with toxaemia of pregnancy* - **Toxemia of pregnancy** (pre-eclampsia/eclampsia) is not directly associated with an increased risk of neonatal hypoglycemia. - However, severe pre-eclampsia can lead to **intrauterine growth restriction (IUGR)** and prematurity, which are indirect risk factors for hypoglycemia due to poor glycogen stores. *Premature infants* - **Premature infants** are at risk for hypoglycemia due to inadequate glycogen stores, immature enzyme systems for gluconeogenesis, and increased metabolic demands. - However, the incidence and severity are less compared to infants of diabetic mothers, where the mechanism involves **active hyperinsulinism** rather than just inadequate reserves.
Question 6: Insulin of choice for the treatment of diabetic ketoacidosis is:
- A. Insulin lispro
- B. Insulin glargine
- C. NPH insulin
- D. Regular Insulin (Correct Answer)
Explanation: ***Regular Insulin*** - **Regular insulin** is the insulin of choice for treating **diabetic ketoacidosis (DKA)** because it can be administered intravenously. - Its **short onset of action** and predictable duration allow for rapid and precise titration in a critical care setting. *Insulin lispro* - **Insulin lispro** is a **rapid-acting insulin analog** typically used for mealtime coverage, which has a very quick onset and short duration. - While it acts quickly, its primary use is not for the continuous intravenous infusion required in DKA management. *Insulin glargine* - **Insulin glargine** is a **long-acting insulin analog** designed to provide basal insulin replacement. - It has a prolonged duration of action and a slow, sustained release profile, making it unsuitable for the rapid correction needed in DKA. *NPH insulin* - **NPH insulin** is an **intermediate-acting insulin** that has a delayed onset and peak effect. - Its insoluble nature and variable absorption make it inappropriate for the acute, immediate intravenous insulin therapy required in DKA.
Question 7: A 28 year female presented to emergency with fever, agitation and delirium. She was on regular medication of Carbimazole 40 mg daily, but missed her doses for the last 2 days. Which of the following scoring systems would you like to do to assess severity of disease?
- A. Sequential Organ Failure Assessment Score
- B. DAS 28 score
- C. Burch-Wartofsky score (Correct Answer)
- D. Expanded Disability Status Scale
Explanation: ***Burch-Wartofsky score*** - The patient's symptoms of **fever, agitation, and delirium** following missed carbimazole doses are highly suggestive of **thyroid storm** [1]. - The **Burch-Wartofsky score** is specifically designed to assess the **likelihood and severity of thyroid storm**, evaluating symptoms related to thermoregulation, central nervous system, gastrointestinal/hepatic dysfunction, cardiovascular dysfunction, and precipitating factors. *Sequential Organ Failure Assessment Score* - The **SOFA score** is used to track the progression of organ dysfunction and predict mortality in critically ill patients, often in the context of **sepsis or general critical illness**. - While thyroid storm can lead to multi-organ dysfunction, the SOFA score does not specifically diagnose or assess the severity of **thyroid storm** itself. *DAS 28 score* - The **DAS28 (Disease Activity Score 28)** is a validated tool for measuring disease activity in patients with **rheumatoid arthritis**. - It assesses joint count, patient global assessment, and inflammatory markers, which are irrelevant to the clinical picture of **fever and delirium**. *Expanded Disability Status Scale* - The **Expanded Disability Status Scale (EDSS)** is a method of quantifying disability in **multiple sclerosis**. - It evaluates neurological function in various systems and is not applicable to an acute presentation of **fever, agitation, and delirium** [2].
Question 8: What is the primary effect of beta blockers in the management of thyroid storm?
- A. Increases metabolism of thyroxine
- B. Blocks thyroxine receptors
- C. Decreases synthesis of thyroxine
- D. Provides rapid relief of symptoms (Correct Answer)
Explanation: Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].
Question 9: A young patient presented with hypertension and a 24-hour urinary metanephrine level of 1.4 mg, the most likely causes are -
- A. Grave's disease
- B. Pseudohypoparathyroidism
- C. Medullary carcinoma thyroid
- D. VonHippelLindau syndrome (Correct Answer)
Explanation: ***Von Hippel-Lindau syndrome*** - This syndrome is a **hereditary condition** predisposing individuals to various tumors, including **pheochromocytomas**, which cause elevated **metanephrines** and hypertension. - The combination of **hypertension** in a young patient and an elevated **24-hour urinary metanephrine level** (indicating excessive catecholamine production) strongly suggests a pheochromocytoma, which is frequently associated with Von Hippel-Lindau syndrome. *Medullary carcinoma thyroid* - This cancer is associated with **MEN 2 syndromes** and produces **calcitonin**, leading to hypocalcemia, but not typically elevated metanephrines or hypertension directly from the thyroid. - While it can be associated with **pheochromocytoma** (as part of MEN 2), it is not the direct cause of the elevated metanephrines. *Grave's disease* - **Grave's disease** is an autoimmune disorder causing **hyperthyroidism**, characterized by symptoms like goiter, exophthalmos, and weight loss. - While it can cause hypertension due to increased cardiac output, it does not lead to elevated **urinary metanephrine levels**, which are specific to catecholamine excess. *Pseudohypoparathyroidism* - This is a genetic disorder characterized by **target organ resistance to parathyroid hormone (PTH)**, leading to hypocalcemia and hyperphosphatemia [1]. - It does not cause hypertension or elevated **urinary metanephrine levels**.
Question 10: Which of the following statements about pheochromocytoma is true?
- A. Arises from chromaffin cells of adrenal medulla (Correct Answer)
- B. Bilateral in 20% of all cases
- C. Hypotension rules out pheochromocytoma
- D. Almost always a malignant tumor
Explanation: ***Arises from chromaffin cells of adrenal medulla*** - **Pheochromocytomas** are rare neuroendocrine tumors that develop from **chromaffin cells** found in the adrenal medulla. - These cells are responsible for synthesizing and secreting **catecholamines**, explaining the characteristic symptoms of pheochromocytoma. *Bilateral in 20% of all cases* - While pheochromocytomas can be bilateral, this occurs in about **10% of cases**, mostly associated with genetic syndromes like **MEN 2**. - A higher percentage of bilaterality is seen in **familial forms** of the disease, but not in all cases. *Hypotension rules out pheochromocytoma* - Although **hypertension** is a hallmark symptom, **hypotension** can occur, particularly **orthostatic hypotension** due to volume depletion and impaired vasoconstriction. - Rarely, **pheochromocytoma crisis** can present with **shock** due to massive catecholamine release and subsequent myocardial dysfunction or vasoplegia. *Almost always a malignant tumor* - Most pheochromocytomas are **benign**; only about **10-15%** are malignant. - Malignancy is suggested by the presence of **metastatic disease**, as histology alone cannot reliably differentiate between benign and malignant forms.
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