NEET-PG 2015 Practice Questions

Q: Which of these is not a part of extracellular matrix:

Integrins. ***Integrins*** - Integrins are **transmembrane receptors** on the cell surface that facilitate cell-extracellular matrix (ECM) adhesion and cell-cell adhesion. - They are part of the cell membrane, **not** an extracellular component. *Laminin* - **Laminin** is a major protein component of the **basal lamina**, a specialized extracellular matrix that underlies epithelial cells. - It plays a crucial role in cell adhesion, differentiation, and migration within the ECM. *Fibronectin* - **Fibronectin** is a large glycoprotein present in the **extracellular matrix** and in soluble form in blood plasma. - It mediates cell adhesion to the ECM by binding to integrins and various ECM components like collagen and proteoglycans. *Collagen* - **Collagen** is the most abundant protein in the human body and a primary structural component of the **extracellular matrix**. - It provides tensile strength and structural integrity to tissues like skin, bone, tendons, and cartilage.

Q: Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?

Hyperkalemia. 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.

Q: Most common cause of Addison's Disease in India is:

Tuberculosis. ***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.

Q: Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?

Sodium levels may appear to increase. ***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.

Q: What condition is characterized by hypertension and hypokalemia?

Liddle's Syndrome. ***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**.

Q: Which of the following is the MOST common condition caused by hypernatremia?

Seizure. ***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]

Q: Which of the following symptoms is least likely to be associated with hyponatremia?

Myalgia. Myalgia - While muscle cramps can occur with electrolyte imbalances, generalized myalgia (muscle pain) is not a typical or primary symptom of hyponatremia. - Hyponatremia primarily affects neurological function due to osmotic shifts in the brain. anorexia - Anorexia (loss of appetite) is a common, non-specific symptom of many metabolic disturbances, including hyponatremia, and often accompanies nausea and vomiting. - It arises from the general malaise and gastrointestinal upset associated with the condition. Convulsions - Convulsions are a severe neurological symptom of acute and profound hyponatremia, resulting from cerebral edema and increased intracranial pressure [1]. - This occurs when the brain swells due to the osmotic shift of water into brain cells. Drowsiness - Drowsiness is a frequent neurological manifestation of hyponatremia, indicative of altered mental status [1]. - It reflects impaired brain function due to the osmotic disturbances and potential cerebral edema [1].

Q: Hyperpigmentation is seen with which hormone?

ACTH. ***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**.

Q: A patient involved in an accident presents with unconsciousness. Upon physical examination, there is unilateral pupillary dilatation. What is the most likely cause of this finding?

Uncal herniation. ***Uncal herniation*** - **Uncal herniation** compresses the **ipsilateral oculomotor nerve (CN III)**, leading to **pupillary dilation** due to predominant parasympathetic fiber damage [1], [2]. - This condition occurs when the **medial temporal lobe (uncus)** is forced over the tentorial notch, often as a result of a **supratentorial mass effect** [2]. *Tonsillar herniation* - **Tonsillar herniation** is the downward displacement of the **cerebellar tonsils** through the **foramen magnum** [1], [2]. - This compression primarily affects the **brainstem** and **cardiorespiratory centers**, causing **respiratory arrest** or **cardiac dysfunction**, not direct pupillary dilation [1]. *Cingulate herniation* - **Cingulate herniation** involves the displacement of the **cingulate gyrus** under the **falx cerebri**. - While it can lead to **hydrocephalus** and **cognitive changes**, it does not directly cause **unilateral pupillary dilation**. *Transcalvarial herniation* - **Transcalvarial herniation** occurs when **brain tissue** extends through a **skull defect** (e.g., following a craniectomy or skull fracture). - This type of herniation is typically visible externally and does not inherently cause **unilateral pupillary dilation** through direct nerve compression.

Question 1

Which of these is not a part of extracellular matrix:

Accepted Answer

Integrins

Answer

Collagen

Answer

Laminin

Answer

Fibronectin

Question 2

Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?

Accepted Answer

Hyperkalemia

Answer

Diastolic Hypertension without edema

Answer

Low Plasma Renin Activity

Answer

Hyperaldosteronism which is not suppressed by volume expansion

Question 3

Most common cause of Addison's Disease in India is:

Accepted Answer

Tuberculosis

Answer

Autoimmune

Answer

HIV

Answer

Malignancy

Question 4

Female with blood sugar of 600 mg% and sodium of 110 mEq. Insulin was given, what will happen to serum sodium levels ?

Accepted Answer

Sodium levels may appear to increase

Answer

Sodium levels decrease

Answer

Sodium levels remain unchanged

Answer

Relative sodium deficiency may occur

Question 5

What condition is characterized by hypertension and hypokalemia?

Accepted Answer

Liddle's Syndrome

Answer

Gitelman's Syndrome

Answer

Bartter Syndrome

Answer

All of the options

Question 6

Which of the following is the MOST common condition caused by hypernatremia?

Accepted Answer

Seizure

Answer

Altered mental status

Answer

Brain hemorrhage

Answer

Central pontine myelinosis

Question 7

Which of the following symptoms is least likely to be associated with hyponatremia?

Accepted Answer

Myalgia

Answer

anorexia

Answer

Drowsiness

Answer

Convulsions

Question 8

Hyperpigmentation is seen with which hormone?

Accepted Answer

ACTH

Answer

TSH

Answer

FSH

Answer

LH

Question 9

A patient involved in an accident presents with unconsciousness. Upon physical examination, there is unilateral pupillary dilatation. What is the most likely cause of this finding?

Accepted Answer

Uncal herniation

Answer

Tonsillar herniation

Answer

Cingulate herniation

Answer

Transcalvarial herniation

Question 10

A 35 year old male came with jaundice, palpable mass in the right hypochondrium not associated with pain. The probable diagnosis is -

Accepted Answer

Pancreatic head carcinoma

Answer

Hepatocellular carcinoma

Answer

Choledochal cyst

Answer

Acute cholecystitis

NEET-PG 2015

Biochemistry

Internal Medicine

Physiology

Surgery