Krebs Cycle Mnemonic for NEET PG: Steps, Enzymes, and Clinical Correlations

The Krebs cycle (citric acid cycle / TCA cycle) shows up in Biochemistry questions less as "name the intermediates" and more as "which enzyme is inhibited here, and what’s the clinical consequence." Knowing the sequence is step one; knowing where the classic poisons and deficiencies act is what actually answers the exam question.

The 8 Steps, in Order

Step	Intermediate	Enzyme
1	Citrate	Citrate synthase
2	Isocitrate	Aconitase
3	α-Ketoglutarate	Isocitrate dehydrogenase
4	Succinyl-CoA	α-Ketoglutarate dehydrogenase
5	Succinate	Succinyl-CoA synthetase
6	Fumarate	Succinate dehydrogenase
7	Malate	Fumarase
8	Oxaloacetate	Malate dehydrogenase

A simple way to hold the order: Citrate, Is, Krebs’, Special, Sauce, For, Making, Oxaloacetate — the first letters (C-I-K-S-S-F-M-O) retrace the same eight intermediates in sequence.

Where It Happens and What It Yields

The cycle runs in the mitochondrial matrix. One turn of the cycle, starting from one acetyl-CoA, produces 3 NADH, 1 FADH2, and 1 GTP (or ATP), along with 2 CO2. Through the electron transport chain, each NADH yields roughly 2.5 ATP and each FADH2 roughly 1.5 ATP — putting the total energy yield per acetyl-CoA at around 10 ATP.

The Rate-Limiting Steps

Three enzymes are considered the key regulatory points: citrate synthase, isocitrate dehydrogenase, and α-ketoglutarate dehydrogenase. These are the steps most sensitive to feedback inhibition by ATP and NADH — and, not coincidentally, the steps most frequently featured in clinical-correlation questions.

Clinical Correlations Worth Knowing

• Arsenic poisoning inhibits α-ketoglutarate dehydrogenase — a thiamine-dependent enzyme, mechanistically similar to how arsenic affects pyruvate dehydrogenase.
• Fluoroacetate/fluorocitrate poisoning inhibits aconitase, a phenomenon classically called "lethal synthesis" because fluoroacetate itself is harmless until it’s converted into fluorocitrate inside the cycle.
• Thiamine (B1) deficiency impairs both pyruvate dehydrogenase and α-ketoglutarate dehydrogenase, since both are thiamine pyrophosphate–dependent — this is part of why thiamine deficiency (as in Wernicke’s encephalopathy) has such wide-reaching metabolic effects.

Metabolic pathway questions like this reward pattern recall over rote memorization — exactly what Reflex’s daily TROCAR Biochemistry rounds are built to drill.