Purine Metabolism Tournament
Two onboarding diagrams orient you in nucleotide metabolism + the de novo / salvage / catabolism architecture. Then eight MCAT-DoK quiz rounds: glutamine-PRPP amidotransferase as committed enzyme, Lesch-Nyhan from HGPRT loss, ADA / PNP immunodeficiencies, the AMP -> hypoxanthine -> uric acid path, allopurinol mechanism, and tumor-lysis pathophysiology.
Where the Metabolism of nucleotides fits in Whole-cell metabolism overview
Purine metabolism builds and recycles A and G ring systems. The de novo path is energy-expensive (~6 ATP per IMP); the salvage path (HGPRT, APRT) is cheap and clinically critical (Lesch-Nyhan if HGPRT fails). Catabolism converges on uric acid - the substrate for gout and tumor lysis. Click the highlighted Metabolism of nucleotides box to enter the tournament.
Click the highlighted Metabolism of nucleotides box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor purine metabolism inside whole-cell metabolism on the live Reactome map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways purine pathway figure before you start answering.
Fill in the Blank
Recall glutamine-PRPP amidotransferase as the committed step (feedback inhibited by AMP/GMP/IMP).
Disruptor
Diagnose Lesch-Nyhan from HGPRT loss + self-mutilation + hyperuricemia + dystonia.
Sequence Ordering
Trace AMP -> adenosine -> inosine -> hypoxanthine -> xanthine -> uric acid (with the right enzyme at each arrow).
Match the Pairs
Pair each enzyme/drug (PRPP synthetase, HGPRT, APRT, allopurinol, probenecid, pegloticase) with its precise role.
Numeric Input
Estimate the ~6 ATP equivalents needed per de novo IMP synthesis.
Select All That Apply
Identify TRUE facts about uricase loss in humans, oxypurinol, allopurinol + 6-MP interaction, and Lesch-Nyhan limits of allopurinol therapy.
Odd One Out
Distinguish purines (A, G, hypoxanthine) from cytosine (a pyrimidine).
Tumor Lysis Disruptor
Predict the K+ / phosphate / Ca2+ / urate cascade that drives AKI in chemotherapy initiation.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Purines in 60 seconds
Purines (A, G, hypoxanthine, xanthine) have two fused rings - built directly on PRPP through 11 enzymatic steps in the de novo path. The committed step is glutamine-PRPP amidotransferase, feedback-inhibited by AMP, GMP, and IMP.
Salvage uses HGPRT (hypoxanthine + guanine) and APRT (adenine) - both consume PRPP and generate the corresponding nucleotide directly. Salvage is energetically far cheaper than de novo synthesis (~1 vs ~6 ATP per nucleotide), which is why deeply quiescent / immune cells rely on it.
Catabolism funnels through hypoxanthine -> xanthine -> uric acid via xanthine oxidase. Humans lack uricase - so we end at uric acid, where most other mammals continue to allantoin. Allopurinol (and oxypurinol) inhibit XO.
Two clinical extremes: Lesch-Nyhan (HGPRT loss -> neurobehavioral phenotype + hyperuricemia, X-linked) and tumor lysis syndrome (chemotherapy unleashes massive purine catabolism -> AKI from urate crystals). Prophylaxis: hydration + allopurinol or rasburicase.
FAQ
Why does allopurinol potentiate 6-MP / azathioprine toxicity?
6-MP is normally inactivated by xanthine oxidase. Allopurinol blocks XO, so 6-MP accumulates and produces severe pancytopenia. If both must be given, dose 6-MP at 25-33% of normal. Use this drug-drug interaction trap as a question-killer.
Why doesn't allopurinol cure Lesch-Nyhan's behavioral symptoms?
Allopurinol blocks the conversion of hypoxanthine to xanthine -> lower urate, no gout. But the neurobehavioral phenotype seems to require salvage-derived IMP/GMP that allopurinol cannot replace. Some evidence suggests dopaminergic dysfunction independent of uric acid.
Why does ADA deficiency cause SCID?
ADA loss causes deoxyadenosine to accumulate, which is phosphorylated to dATP. dATP allosterically inhibits ribonucleotide reductase, depleting other dNTPs and preventing DNA synthesis. Lymphocytes (especially T cells) are most sensitive due to their proliferative demands.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.