Which of the following can cause hypoglycaemia in a patient of severe cerebral malaria on treatment?
First, I should recall the causes of hypoglycemia in malaria. Severe malaria, especially cerebral, is associated with several metabolic disturbances. One key point is that the body's stress response can increase glucose utilization. Also, some antimalarial drugs might affect glucose metabolism.
Quinine, which is used in treating malaria, can cause hypoglycemia. I remember that quinine inhibits gluconeogenesis and increases insulin release, leading to lower blood sugar. That's a possible culprit here. Another drug might be artemisinin derivatives, but I'm not sure if they have the same effect. Let me check that.
Other factors in cerebral malaria include lactic acidosis and hepatic dysfunction, which can impair glucose production. So if the patient is on a drug that exacerbates this, hypoglycemia is more likely. Quinine is known for causing hypoglycemia, especially in severe cases. So the correct answer would be Quinine.
Now, the options might include other medications or factors. The incorrect options could be other antimalarials like chloroquine, which doesn't cause hypoglycemia. Or maybe factors like dehydration or concurrent infections, but the question specifies the treatment. So the wrong options would be other drugs or unrelated causes.
The clinical pearl here is to remember that quinine can cause hypoglycemia, and in cerebral malaria patients, monitoring blood glucose is crucial. Also, hypoglycemia in this context is a known complication due to both disease and treatment.
**Core Concept**
Severe cerebral malaria induces metabolic stress and impaired hepatic gluconeogenesis. Hypoglycaemia in this context is often drug-induced, particularly with antimalarials that enhance insulin secretion or inhibit glucose production. **Quinine** is a high-yield culprit due to its direct pancreatic and hepatic effects.
**Why the Correct Answer is Right**
**Quinine** causes hypoglycaemia by:
1. **Stimulating insulin release** from pancreatic β-cells via activation of ATP-sensitive K+ channels.
2. **Inhibiting gluconeogenesis** in the liver by reducing glycogenolysis and gluconeogenic enzyme activity (e.g., glucose-6-phosphatase).
3. **Increasing peripheral glucose uptake** in muscle and adipose tissue.
These mechanisms are exacerbated in cerebral malaria due to pre-existing hepatic dysfunction and metabolic acidosis.
**Why Each Wrong Option is Incorrect**
**Option A:** **Chloroquine** does not cause hypoglycaemia; it stabilizes lysosomal membranes but has no direct effect on glucose metabolism.
**Option B:** **Artemisinin derivatives** (e.g., artemether) are less likely to induce hypoglycaemia compared to quinine.
**Option C:** **Paracetamol** is not a first-line antimalarial and does not affect glucose homeostasis.
**Clinical Pearl / High-Yield Fact**
Never administer **quinine** without concurrent glucose monitoring in severe malaria. Hypoglycaemia is a classic "trap" in NEET PG