Thrombocythemia is characterized by an elevated platelet count.
In a patient with hypoglycemia, what is the appropriate dose adjustment of insulin?
What is the best indicator for assessing short-term control of blood glucose levels over a period of 2-3 weeks?
What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?
Hyperpigmentation is seen with which hormone?
Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?
Most common cause of Addison's Disease in India is:
Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?
What condition is characterized by hypertension and hypokalemia?
Which of the following is the MOST common condition caused by hypernatremia?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 61: Thrombocythemia is characterized by an elevated platelet count.
- A. Low platelets
- B. Neutrophilia
- C. Monocytosis
- D. Elevated platelet count (Correct Answer)
Explanation: Elevated platelet count - Thrombocythemia is a condition specifically defined by an abnormally high number of platelets (thrombocytes) in the blood [2]. - This elevated count can lead to issues with both bleeding and clotting [2]. Low platelets - Low platelets, also known as thrombocytopenia, is the opposite of thrombocythemia [1]. - This condition is associated with an increased risk of bleeding [1]. Neutrophilia - Neutrophilia refers to an elevated count of neutrophils, a type of white blood cell, which is typically seen in bacterial infections. - It does not directly describe the platelet count. Monocytosis - Monocytosis indicates an increase in monocytes, another type of white blood cell, often seen in chronic infections or inflammatory conditions. - This term is unrelated to platelet levels.
Question 62: In a patient with hypoglycemia, what is the appropriate dose adjustment of insulin?
- A. Increase insulin dosage
- B. Decrease insulin dosage (Correct Answer)
- C. Maintain current insulin dosage
- D. Add a different medication
Explanation: ***Decrease insulin dosage*** - Hypoglycemia indicates that the current insulin dose is too high, causing blood glucose levels to drop excessively [1]. - Reducing the insulin dosage helps prevent future episodes of low blood sugar by allowing blood glucose to remain within a healthier range [1]. *Increase insulin dosage* - Increasing insulin would further lower blood glucose, exacerbating the **hypoglycemia** and potentially leading to a more severe and dangerous state. - This action is appropriate for **hyperglycemia**, not hypoglycemia. *Maintain current insulin dosage* - Maintaining the current dose would not address the problem, as it has already proven to be too much for the patient, causing the **hypoglycemic episodes** [1]. - This approach would leave the patient at continued risk for recurrent hypoglycemia. *Add a different medication* - While other medications might be used in diabetes management, adding a new one without adjusting the existing insulin dose could further complicate blood glucose control. - The immediate and most direct action for **hypoglycemia** caused by insulin is to adjust the insulin itself [1].
Question 63: What is the best indicator for assessing short-term control of blood glucose levels over a period of 2-3 weeks?
- A. Serum fructosamine (Correct Answer)
- B. Blood sugar
- C. Urine sugar
- D. HbA1c
Explanation: ***Serum fructosamine*** - **Fructosamine** reflects the glycation of serum proteins, primarily albumin, which has a shorter half-life (around 17-20 days) compared to hemoglobin. - This allows it to assess average blood glucose control over the preceding **2-3 weeks**, making it suitable for short-term monitoring. *HbA1c* - **HbA1c** (glycated hemoglobin) reflects average blood glucose levels over the lifespan of red blood cells, typically **2-3 months** [1]. - While an excellent long-term indicator, its longer time frame makes it less suitable for assessing short-term changes over just 2-3 weeks [1]. *Blood sugar* - A single **blood sugar** measurement (fasting or random) provides an instantaneous snapshot of glucose levels at that specific moment [2]. - It does not reflect average glucose control over a period of 2-3 weeks and is highly influenced by recent food intake and activity [2]. *Urine sugar* - **Urine sugar** levels indicate that the kidney's reabsorption capacity for glucose has been exceeded, resulting in glucose spilling into the urine [3]. - This is a qualitative or semi-quantitative measure that primarily reflects very high blood glucose levels and is not a reliable indicator of averaged glucose control over any specific time frame [3].
Question 64: What is the recommended postprandial capillary glucose level (in mg/dl) for adequate diabetes control?
- A. < 180 mg/dl (Correct Answer)
- B. < 200 mg/dl
- C. < 100 mg/dl
- D. < 140 mg/dl
Explanation: ***< 180 mg/dl*** - This is the **recommended target** for postprandial (1-2 hours after a meal) capillary glucose levels in most non-pregnant adults with diabetes to achieve **adequate glycemic control** [1], [2]. - Maintaining levels below 180 mg/dl helps to minimize the risk of **long-term microvascular and macrovascular complications**. *< 100 mg/dl* - While this is an ideal fasting glucose level, it is generally **too low for postprandial glucose**, and attempting to maintain such levels might increase the risk of **hypoglycemia** in many patients with diabetes [1]. - This target is more appropriate for **fasting or pre-meal glucose** goals. *< 140 mg/dl* - This is a **more stringent target** that may be appropriate for some individuals with diabetes, particularly those who are carefully managed and at low risk of hypoglycemia. - However, for the general population with diabetes, **< 180 mg/dl is the more commonly accepted and achievable goal** for postprandial readings [2]. *< 200 mg/dl* - A postprandial glucose level of < 200 mg/dl is considered **good control** in some contexts, but it's often a **less strict target** than < 180 mg/dl for optimal long-term management. - While better than uncontrolled high levels, consistently approaching 200 mg/dl may still contribute to **increased risk of complications** over time compared to tighter control.
Question 65: Hyperpigmentation is seen with which hormone?
- A. TSH
- B. ACTH (Correct Answer)
- C. FSH
- D. LH
Explanation: ***ACTH*** - In conditions like **Addison's disease**, the adrenal glands' inability to produce cortisol leads to increased **ACTH** (adrenocorticotropic hormone) secretion due to a lack of negative feedback [3], [4]. - ACTH is derived from proopiomelanocortin (POMC), which also gives rise to alpha-melanocyte-stimulating hormone (α-MSH). Elevated ACTH levels can thus stimulate melanocytes, causing **hyperpigmentation** in skin folds, buccal mucosa, and pressure points [4]. *FSH* - **FSH** (follicle-stimulating hormone) primarily regulates the development of **follicles in the ovaries** and sperm production in the testes [1]. - There is no known direct association between excessive FSH levels and **hyperpigmentation**. *TSH* - **TSH** (thyroid-stimulating hormone) stimulates the **thyroid gland** to produce thyroid hormones (T3 and T4) [1]. - While thyroid disorders can affect skin texture and moisture, there is no direct link between elevated TSH and **hyperpigmentation**. *LH* - **LH** (luteinizing hormone) plays a key role in **ovulation** in females and testosterone production in males [2]. - High LH levels are not associated with **hyperpigmentation**.
Question 66: Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?
- A. Diastolic Hypertension without edema
- B. Low Plasma Renin Activity
- C. Hyperkalemia (Correct Answer)
- D. Hyperaldosteronism which is not suppressed by volume expansion
Explanation: Primary hyperaldosteronism is typically characterized by **hypokalemia** due to excessive aldosterone-mediated potassium excretion in the urine, not hyperkalemia [1]. Hyperkalemia would suggest other conditions, such as **adrenal insufficiency** or kidney disease, rather than primary hyperaldosteronism [2]. *Diastolic Hypertension without edema* - **Diastolic hypertension** is a common presentation of primary hyperaldosteronism due to increased **sodium and water retention**, leading to expanded extracellular volume. - The absence of significant edema is also common, as the body often develops an **"escape phenomenon"** where natriuresis occurs despite high aldosterone, preventing overt fluid overload [3]. *Low Plasma Renin Activity* - In primary hyperaldosteronism, the high aldosterone levels **suppress renin secretion** through negative feedback mechanisms. - Therefore, a **low plasma renin activity** (PRA) or plasma renin concentration (PRC) is a key diagnostic feature [4]. *Hyperaldosteronism which is not suppressed by volume expansion* - Normally, volume expansion would suppress aldosterone secretion. However, in primary hyperaldosteronism, aldosterone production is **autonomous** and remains elevated even after volume expansion. - This lack of suppression is a critical diagnostic criterion, often assessed through various **confirmatory tests** like saline infusion or oral sodium loading.
Question 67: Most common cause of Addison's Disease in India is:
- A. Autoimmune
- B. HIV
- C. Tuberculosis (Correct Answer)
- D. Malignancy
Explanation: ***Tuberculosis*** - In India, **tuberculosis** is the most common cause of **Addison's disease** due to the high prevalence of TB infections. - Adrenal involvement in TB can lead to gradual destruction of the adrenal cortex, resulting in **adrenal insufficiency**. *Autoimmune* - **Autoimmune adrenalitis** is the leading cause of Addison's disease in developed Western countries. - It involves the destruction of adrenal cortical cells by the body's own immune system, often associated with other autoimmune conditions. *Malignancy* - **Malignancy**, particularly metastatic cancer to the adrenals, can cause adrenal insufficiency but is a less common primary cause of Addison's disease overall. - While possible, it is not the most prevalent cause in India compared to infectious etiologies. *HIV* - **HIV infection** can lead to adrenal dysfunction, but it's typically through opportunistic infections like CMV, cryptococcosis, or direct HIV effects, rather than being the direct cause of widespread adrenal destruction. - It increases the risk of adrenal insufficiency but is not the most common etiology in India for Addison's disease.
Question 68: Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?
- A. Sodium levels may appear to increase (Correct Answer)
- B. Sodium levels decrease
- C. Sodium levels remain unchanged
- D. Relative sodium deficiency may occur
Explanation: ***Sodium levels may appear to increase*** - The patient's initial presentation with severe hyperglycemia (600 mg%) and hyponatremia (110 mEq/L) suggests **hyperglycemia-induced pseudohyponatremia**. - **Insulin administration** will lower blood glucose, causing water to shift back into the cells from the extracellular space, thereby correcting the dilutional effect and leading to an **apparent increase in serum sodium levels**. *Sodium levels decrease* - This is incorrect because the hyponatremia in this scenario is largely **dilutional** due to hyperglycemia. - As glucose levels decrease with insulin, the osmotic drive for water movement out of cells diminishes, leading to **normalization**, not further decrease, of sodium concentration. *Sodium levels remain unchanged* - This is incorrect because the underlying cause of the initial low sodium is dilution from high glucose. - Once **hyperglycemia is treated**, the osmotic gradient changes, and water shifts, directly impacting and changing the serum sodium concentration. *Relative sodium deficiency may occur* - This option is incorrect because the initial hyponatremia is not primarily due to an absolute lack of sodium in the body but rather a **dilutional effect** caused by the osmotic pull of glucose. - As hyperglycemia resolves, the extracellular fluid becomes less diluted, and the measured sodium concentration will **rise**, not indicate a deficiency.
Question 69: What condition is characterized by hypertension and hypokalemia?
- A. Gitelman's Syndrome
- B. Liddle's Syndrome (Correct Answer)
- C. Bartter Syndrome
- D. All of the options
Explanation: ***Liddle's Syndrome*** - This syndrome is characterized by **overactivity of the epithelial sodium channel (ENaC)** in the collecting ducts, leading to increased sodium reabsorption and potassium excretion. [1] - The resulting **sodium retention causes hypertension**, while the **potassium excretion leads to hypokalemia**. *Gitelman's Syndrome* - This is an **autosomal recessive kidney disorder** causing a defect in the **thiazide-sensitive NaCl cotransporter** in the distal convoluted tubule. - It presents with **hypokalemia and hypomagnesemia**, but typically with **normal or low blood pressure**, not hypertension. *Bartter Syndrome* - This is a group of **autosomal recessive salt-wasting tubulopathies** affecting the **Na-K-2Cl cotransporter** in the thick ascending limb of the loop of Henle. - It leads to **hypokalemia, metabolic alkalosis, and normal or low blood pressure**, similar to chronic loop diuretic use. *All of the options* - While all mentioned conditions involve **hypokalemia**, only **Liddle's Syndrome** is consistently associated with **hypertension**. - **Gitelman's and Bartter syndromes** typically present with **normal or low blood pressure**.
Question 70: Which of the following is the MOST common condition caused by hypernatremia?
- A. Altered mental status
- B. Brain hemorrhage
- C. Seizure (Correct Answer)
- D. Central pontine myelinosis
Explanation: ***Seizure*** - While not the *most* common initial symptom, **seizure** can be a severe manifestation of hypernatremia, particularly when the serum sodium levels rise rapidly or to very high concentrations leading to significant neuronal dehydration. - **Rapid correction of severe hypernatremia** can also induce seizures if the brain cells swell too quickly. *Altered mental status* - **Altered mental status** such as lethargy, confusion, or irritability, is a very common and often an earlier symptom of hypernatremia due to neuronal dehydration and intracellular water shifts, but it generally precedes more severe neurological complications like seizures.[1] - It is a broad term that encompasses a range of neurological dysfunctions, and while frequent, it is not as specific a severe endpoint as a seizure. *Brain hemorrhage* - **Brain hemorrhage** is a rare and severe complication of hypernatremia, primarily seen when extreme osmotic shifts cause significant brain shrinkage, leading to tension on bridging veins and potential rupture. - This is not a common presentation and typically occurs only in very severe cases of hypernatremia or during overly rapid correction. *Central pontine myelinosis* - **Central pontine myelinolysis (CPM)** is a neurological disorder caused by too rapid correction of *chronic hyponatremia*, not hypernatremia.[1] - It results from osmotic damage to myelin sheaths in the pons, leading to severe neurological deficits such as dysphagia, dysarthria, and even locked-in syndrome.[1]