Physiology, MBBS Second Year. This chapter is split into 10 topics and has
400 practice questions. The topics covered are listed below, followed by
10 free sample questions from the chapter.
Sample questions: Insulin, Glucagon, and Diabetes Mellitus
10 sample questions with the correct answer and an explanation. Try to answer each one before reading the explanation.
Q1. Why does insulin deficiency cause both hyperglycaemia and hypoglycaemic symptoms in the brain?
A. Because the brain uses only fatty acids
B. Because insulin deficiency increases brain glucose uptake
C. Because the brain requires insulin for glucose uptake
D. Because glucose accumulates in the blood while failing to enter insulin-dependent tissues, and although the brain does not need insulin for glucose uptake, its function depends on adequate blood glucose(correct answer)
Answer: D.In insulin deficiency glucose cannot enter insulin-dependent tissues such as muscle and fat, so it accumulates in the blood (hyperglycaemia); the brain does not require insulin to take up glucose, but its function depends on the blood glucose concentration, so hypoglycaemia (for example from excess insulin) depresses CNS function.
Q2. Which sequence correctly describes the mechanism of insulin secretion?
A. Glucose enters the beta cell via GLUT-2 → glucokinase phosphorylates it to glucose-6-phosphate → oxidation generates ATP → the ATP-sensitive K+ channel closes → depolarization → Ca2+ channels open → Ca2+ influx → insulin secretion(correct answer)
B. Glucose binds the insulin receptor → cAMP → insulin secretion
C. Glucose opens K+ channels → hyperpolarization → insulin secretion
D. Glucose is converted to insulin directly
Answer: A.Glucose enters the beta cell through GLUT-2 and is phosphorylated by glucokinase; oxidation generates ATP, which closes the ATP-sensitive potassium channel, causing depolarization, opening of voltage-gated calcium channels and calcium influx that triggers insulin secretion.
Q3. Which factors increase insulin secretion?
A. Decreased blood glucose and somatostatin
B. Fasting only
C. Alpha-adrenergic activity
D. Increased blood glucose, increased blood free fatty acids, increased blood amino acids, GI hormones, glucagon, growth hormone, cortisol, parasympathetic and beta-adrenergic stimulation, insulin resistance, obesity, sulfonylureas and leptin(correct answer)
Answer: D.Insulin secretion is increased by raised blood glucose, free fatty acids and amino acids; by GI hormones (gastrin, CCK, secretin, GIP, GLP-1); by glucagon, growth hormone and cortisol; by parasympathetic (acetylcholine) and beta-adrenergic stimulation; and by insulin resistance, obesity, sulfonylureas and leptin.
Q4. Why is the reciprocal regulation of insulin and its counter-regulatory hormones essential?
A. Because both hormones raise blood glucose
B. Because both lower blood glucose
C. Because glucose regulation is unnecessary
D. Because opposing signals allow blood glucose to be held within a narrow range whether the person has just eaten or is fasting(correct answer)
Answer: D.Insulin stores fuel and lowers glucose in the fed state, while glucagon, growth hormone, cortisol and epinephrine mobilise fuel and raise glucose in the fasted state; their reciprocal actions keep blood glucose within a narrow range across feeding and fasting.
Q5. Which sequence correctly describes glucagon-induced glycogenolysis?
A. Glucagon directly phosphorylates glycogen
B. Adenylyl cyclase activation in the hepatic cell membrane → cyclic AMP formation → protein kinase regulator protein activation → protein kinase activation → phosphorylase b kinase activation → conversion of phosphorylase b into phosphorylase a → degradation of glycogen into glucose-1-phosphate → dephosphorylation → release of glucose from liver cells(correct answer)
C. Glucagon converts glucose-1-phosphate into glycogen
D. Glucagon inhibits adenylyl cyclase
Answer: B.Glucagon activates adenylyl cyclase in the hepatic cell membrane, forming cyclic AMP; this activates protein kinase, which activates phosphorylase b kinase, converting phosphorylase b to phosphorylase a; glycogen is degraded to glucose-1-phosphate, which is dephosphorylated and released as glucose from the liver cells.
Q6. Why does the body need both rapid and slow responses to hypoglycaemia?
A. Because the acute sympathetic-epinephrine response corrects a fall within minutes, while growth hormone and cortisol provide longer-term adjustments of glucose and fat utilization(correct answer)
B. Because growth hormone acts within seconds
C. Because no rapid response exists
D. Because epinephrine acts only after hours
Answer: A.The acute response to hypoglycaemia is rapid sympathetic activation with epinephrine release stimulating hepatic glucose release; for prolonged hypoglycaemia, growth hormone and cortisol act more slowly to decrease glucose utilization and promote fat utilization, normalizing blood glucose over a longer period.
Q7. Which features constitute the metabolic syndrome?
A. Obesity (especially abdominal fat), insulin resistance, fasting hyperglycaemia, dyslipidaemia (elevated triglycerides, low HDL cholesterol) and hypertension(correct answer)
B. Normal glucose with low triglycerides
C. Weight loss and hypotension
D. Isolated high HDL cholesterol
Answer: A.The metabolic syndrome includes obesity (especially abdominal fat), insulin resistance, fasting hyperglycaemia, dyslipidaemia with elevated triglycerides and low HDL cholesterol, and hypertension; it is strongly linked to excess adipose tissue and visceral fat.
Q8. Why does treating insulin resistance improve both glucose control and cardiovascular risk in type 2 diabetes?
A. Because insulin resistance is linked to dyslipidaemia, hypertension and visceral obesity, so reducing it improves lipids, blood pressure and glucose together(correct answer)
B. Because treatment eliminates the need for lifestyle change
C. Because insulin resistance protects the heart
D. Because insulin resistance affects only glucose
Answer: A.Insulin resistance is the common thread linking hyperglycaemia, dyslipidaemia, hypertension and visceral obesity in the metabolic syndrome; interventions such as weight loss, metformin, thiazolidinediones, GLP-1 mimetics and SGLT2 inhibitors improve glucose control while also benefitting lipids, blood pressure and cardiovascular/kidney outcomes.
Q9. Which statement correctly contrasts the previous and current dietary approaches to diabetes management?
A. Currently severe carbohydrate restriction is recommended
B. Diet has no role in either approach
C. Previously severe carbohydrate restriction was used to lower insulin needs (ineffective for lipid abnormalities), whereas now normal carbohydrate intake with sufficient insulin administration reduces fat metabolism abnormalities and cholesterol levels(correct answer)
D. Previously normal carbohydrate intake was used
Answer: C.The previous approach of severe carbohydrate restriction to lower insulin requirements was ineffective for lipid abnormalities; the current approach uses normal carbohydrate intake with sufficient insulin administration, which reduces fat metabolism abnormalities and cholesterol levels.
Q10. Why do diabetic patients need both glucose-lowering treatment and lipid-lowering treatment?
A. Because diabetes carries increased risk of arteriosclerosis, kidney disease and coronary disease through associated hypertension and lipid abnormalities, not hyperglycaemia alone(correct answer)
B. Because lipids cause hypoglycaemia
C. Because glucose-lowering drugs raise cholesterol
D. Because lipids are the only risk factor
Answer: A.Diabetes increases the risk of arteriosclerosis and kidney disease and accelerates heart disease, with hypertension, high cholesterol and lipid metabolism abnormalities contributing; therefore management combines glucose control with lipid-lowering drugs to prevent complications.