INICET Physiology Previous Year Questions (2017–2026)

The correct answer is B. SGLT-1.

Acute watery diarrhoea (here likely Bacillus cereus from reheated rice) is managed with oral rehydration solution (ORS). ORS works through SGLT-1, the sodium-glucose cotransporter on the apical membrane of enterocytes, which carries 2 sodium ions with 1 glucose molecule into the cell so that water follows by osmosis. This glucose-coupled sodium absorption is preserved even in secretory diarrhoea, so raising SGLT-1 activity maximises sodium and water uptake despite ongoing losses. The tempting distractor is the Na+/K+ ATPase, which does sustain the basolateral sodium gradient that powers SGLT-1, but it is not the glucose-coupled absorptive step ORS exploits, so it is not the answer. This coupling is exactly why ORS pairs glucose with salt.

Why the other options are incorrect:

• A. CFTR: The apical chloride channel that drives secretory diarrhoea. Increasing it would push more chloride and water into the lumen, worsening fluid loss.
• C. Na+/K+ ATPase pump: Maintains the sodium gradient that powers SGLT-1 but is not itself the glucose-coupled absorptive step targeted by ORS.
• D. Na+/H+ exchanger: Nutrient-independent sodium absorption that is actually impaired during diarrhoea, so it cannot be relied on for rehydration.

High-Yield Facts:

• SGLT-1 couples sodium with glucose absorption and is the basis of ORS.
• Sodium-glucose cotransport is preserved in secretory diarrhoea.
• Water follows the absorbed sodium and glucose by osmosis.
• CFTR drives secretory diarrhoea, the opposite of absorption.

The intestinal Na-glucose cotransporter SGLT1 carries sodium with glucose into the enterocyte, with water following by osmosis - the molecular basis of ORS. GLUT2 exports glucose basolaterally, and the Na+/K+ ATPase maintains the sodium gradient.

Summary: boosting SGLT-1 (glucose-coupled, absorptive, diarrhoea-resistant) best aids rehydration. CFTR would worsen secretory loss, the Na+/K+ ATPase only supports the gradient, and the Na+/H+ exchanger is impaired in diarrhoea.

The correct answer is Low pressure developed during right ventricular systole.

Coronary flow is phasic because the contracting myocardium compresses the intramural vessels during systole. The left ventricle generates a high systolic pressure (about 120 mmHg) that strongly compresses the left coronary vessels, so left coronary flow occurs mainly in diastole. The right ventricle develops a much lower systolic pressure (about 25 mmHg) and has a thin wall, so its vessels are barely compressed - therefore right coronary flow continues during both systole and diastole and follows the aortic pressure curve. The difference is thus explained by the low pressure developed during right ventricular systole.

Option C is a trap - the right ventricular wall is in fact thin, not thick, which is exactly why compression is minimal. The dominant, testable explanation among the options is the low systolic pressure of the right ventricle.

Incorrect Options:

• High pressure developed during right ventricular systole: the right ventricle generates low, not high, systolic pressure.
• Thick right ventricular wall: the right ventricular wall is thin - a thick wall would increase, not reduce, compression.
• Reversal of flow during end of atrial systole: not the mechanism of the right-versus-left phasic difference.

High-Yield Facts:

• Left coronary flow is mainly diastolic due to high LV systolic compression.
• Right coronary flow occurs in both systole and diastole (low RV pressure, thin wall).
• Right coronary flow follows the aortic pressure curve.
• Diastolic dependence makes the left heart vulnerable to ischaemia in tachycardia.

Figure: The right (RCA) and left (LCA) coronary arteries. The low-pressure right ventricle compresses the RCA little, so right coronary flow persists in systole, while left coronary flow is mainly diastolic.

The correct answer is Increased glucose uptake by skeletal muscle via GLUT4.

Insulin binds its receptor and triggers the PI3K-Akt pathway, which translocates GLUT4 from intracellular vesicles to the plasma membrane. GLUT4 is the insulin-responsive glucose transporter found in skeletal muscle, cardiac muscle and adipose tissue, so insulin therapy increases glucose uptake into skeletal muscle through GLUT4, lowering blood glucose. The liver instead uses GLUT2, a high-capacity insulin-independent transporter, so hepatic glucose handling is not driven by GLUT4.

The key pairing is GLUT4 with insulin-sensitive muscle and fat, not the liver. Muscle GLUT4 can also be recruited insulin-independently by exercise via the AMP-activated kinase pathway.

Incorrect Options:

• Increased glucose uptake by skeletal muscle via GLUT2: muscle uses GLUT4, not GLUT2, for insulin-stimulated uptake.
• Increased glucose uptake by liver via GLUT4: the liver expresses GLUT2, not GLUT4.
• Increased glucose uptake by liver via GLUT2: GLUT2 is insulin-independent, so insulin does not directly raise hepatic uptake through it.

High-Yield Facts:

• GLUT4 is the insulin-responsive transporter in muscle, heart and adipose tissue.
• Insulin recruits GLUT4 to the membrane via the PI3K-Akt pathway.
• The liver uses insulin-independent GLUT2.
• Exercise recruits GLUT4 independently of insulin via AMP-kinase.

Figure: Insulin binds its receptor and recruits GLUT4 to the membrane, increasing glucose uptake into the cell - the insulin-responsive transporter of muscle and adipose tissue.