Where Each Drug Strikes
Five drugs in one regimen. Each one has a signature organ. Tap a drug to light up its target.
Bleomycin chelates iron and generates free radicals that snap DNA strands. The lungs and skin lack bleomycin hydrolase, the enzyme that inactivates the drug everywhere else, so they accumulate damage and scar. The result is pneumonitis and pulmonary fibrosis: dry cough, bibasilar crackles, low DLCO. Minimal myelosuppression.
Cisplatin cross-links DNA like an alkylator. Its toxicity triad is nephrotoxicity, ototoxicity, and peripheral neuropathy. Prevent kidney damage with aggressive saline hydration plus amifostine. No lung fibrosis. If the question says rising creatinine and ringing ears, this is your drug.
Bevacizumab is a monoclonal antibody against VEGF. Block new vessel growth and you get hypertension, proteinuria, bleeding, impaired wound healing, and thromboembolism. A vascular-signature toxicity, not a lung one.
Paclitaxel hyperstabilizes microtubules so the mitotic spindle cannot break down. Its hallmark toxicity is peripheral sensory neuropathy (stocking-glove numbness) plus hypersensitivity reactions and neutropenia. It does not scar the lungs.
5-Fluorouracil inhibits thymidylate synthase, starving cells of thymidine. Its toxicities cluster in fast-turnover tissue: mucositis, diarrhea, myelosuppression, and hand-foot syndrome. Coronary vasospasm is the sleeper. Not a pulmonary fibrosis drug.
The Regimen Lineup
Tap each card to open the full breakdown: mechanism, signature toxicity, and the antidote that pairs with it.
Bleomycin
Free-Radical DNA Breaker
Trace It
A glycopeptide that chelates iron and makes oxygen free radicals. Those radicals cause DNA strand breaks and stall cells in G2/M phaseBleomycin is cell-cycle specific, acting mainly in the G2 and M phases. The strand breaks trigger checkpoint arrest before mitosis..
Why The Lungs
Most tissues inactivate bleomycin with bleomycin hydrolase. Lung and skin have very little of it, so the drug lingers and scars them.
Signature Toxicity
Pulmonary fibrosis / pneumonitis: dry cough, bibasilar crackles, falling DLCO. Worsened by high inspired oxygen and chest radiation. Skin: hyperpigmentation, flagellate streaks.
The Marrow Clue
Minimal myelosuppression. Normal blood counts beside a scarred lung points here.
Bleomycin = the lung-and-skin drug that spares the marrow. Keep the oxygen low in surgery and watch the DLCO.
Bleomycin structure
Clubbing (chronic fibrosis)
Cisplatin
Platinum Cross-Linker
Trace It
A platinum agent that cross-links DNA between and within strands, behaving like an alkylating agent. Cell-cycle nonspecific.
Signature Toxicity
Nephrotoxicity, ototoxicity, and peripheral neuropathy. Rising creatinine, ringing ears, numb feet. This is the look-alike students confuse with bleomycin.
The Rescue Pair
Protect the kidney with saline hydration plus amifostine (a free-radical scavenger). Hydration is the workhorse.
Cisplatin hits kidney, ear, and nerve. It does NOT scar the lung. Dry cough plus opacities is never cisplatin.
Paclitaxel
Microtubule Stabilizer
Trace It
Hyperstabilizes microtubules so the mitotic spindle cannot disassemble. Cells freeze in mitosis. (Vinca alkaloids do the opposite: they block assembly.)
Signature Toxicity
Peripheral sensory neuropathy, hypersensitivity reactions, and neutropenia. The neuropathy is the board hook.
Taxanes stabilize, vincas destabilize. Both wreck mitosis, neither scars the lung.
Bevacizumab
Anti-VEGF Antibody
Trace It
A monoclonal antibody that binds VEGF, starving the tumor of new blood vessels.
Signature Toxicity
Hypertension, proteinuria, bleeding, impaired wound healing, GI perforation, thromboembolism. A vascular profile.
Block vessels, break vessels. HTN and proteinuria, not a cough.
5-Fluorouracil
Thymidylate Synthase Inhibitor
Trace It
A pyrimidine analog that becomes 5-FdUMP and shuts down thymidylate synthase, cutting off thymidine for DNA.
Signature Toxicity
Mucositis, diarrhea, myelosuppression, hand-foot syndrome. Coronary vasospasm is the surprise.
Fast-turnover tissue suffers: mouth, gut, marrow, palms. Lung is untouched.
Three hooks to lock it in. Tap each to unblur.
Lung, not marrow
Bleomycin and busulfan are the two classic pulmonary-fibrosis chemo drugs. Bleomycin's tell is that the marrow stays normal while the lung scars.
No hydrolase, no mercy
Lung and skin have little bleomycin hydrolase, so the drug is not cleared there. That is exactly why those two tissues take the damage.
Oxygen feeds the fire
High inspired oxygen and chest radiation both potentiate bleomycin lung injury. Anesthesia keeps FiO2 low for these patients.
Spot The Culprit
Work the tree first, then run the elimination drills. Commit to an answer before you reveal.
A patient months out from combination chemotherapy has a dry cough and bibasilar crackles. Before imaging, what is the single most useful next question to separate bleomycin lung injury from a marrow-toxic look-alike?
Counts first. Bleomycin spares the marrow, so normal counts beside lung scarring point at it. Most other cytotoxics that could explain illness would drop the counts. Fever and potassium do not sort bleomycin from its rivals.
Counts are normal and the chest film shows diffuse reticular opacities. Which single bedside test best confirms the pattern of bleomycin injury?
A falling DLCO. Bleomycin scars the alveolar interface, so gas transfer drops early, often before the film looks dramatic. Peak flow tracks airway obstruction, and methacholine challenge tests asthma, not fibrosis.
A 28-year-old man treated for testicular cancer with a bleomycin-containing regimen needs abdominal surgery. The anesthesiologist deliberately keeps the inspired oxygen low and avoids fluid overload. Which agent's toxicity drives this precaution?
Bleomycin
Cisplatin
Etoposide
Vincristine
Clue 1: Only one of these drugs has a toxicity that high inspired oxygen makes worse.
Clue 2: Cisplatin harms kidney, ear, and nerve. Oxygen does not change that. Eliminated.
Clue 3: Etoposide and vincristine cause myelosuppression and neuropathy respectively. Neither is oxygen-potentiated. Eliminated.
Clue 4: Bleomycin generates oxygen free radicals. More oxygen means more radicals means more lung scarring. Keep FiO2 low.
Bleomycin. Its lung injury runs on oxygen free radicals, so supplemental oxygen and fluid overload both feed the damage. Anesthesia keeps FiO2 at the minimum that maintains saturation.
A patient on multi-agent chemotherapy returns with rising creatinine, ringing in the ears, and numb feet. The lungs are clear. Which agent is responsible?
Cisplatin
Bleomycin
Bevacizumab
5-Fluorouracil
Clue 1: The triad of kidney, ear, and nerve damage is one drug's calling card.
Clue 2: Bleomycin scars the lungs, but here the lungs are clear. Eliminated.
Clue 3: Bevacizumab causes hypertension and proteinuria. 5-FU causes mucositis and hand-foot syndrome. Neither gives ototoxicity. Eliminated.
Clue 4: Nephrotoxicity plus ototoxicity plus peripheral neuropathy is cisplatin until proven otherwise.
Cisplatin. The platinum triad is nephrotoxicity, ototoxicity, and peripheral neuropathy. This is the reverse-discrimination case: same regimen, different organ, different drug.
During a regimen for Hodgkin lymphoma, serial pulmonary function tests show a steadily falling DLCO while the white count, hemoglobin, and platelets stay normal. Which agent should be held?
Doxorubicin
Bleomycin
Vinblastine
Dacarbazine
Clue 1: A falling DLCO with normal counts isolates a lung-specific, marrow-sparing drug.
Clue 2: Doxorubicin's signature is dilated cardiomyopathy, and it suppresses the marrow. Eliminated.
Clue 3: Vinblastine and dacarbazine both lower blood counts. The normal counts here rule them out.
Clue 4: A dropping DLCO with a clean marrow is bleomycin lung toxicity. Hold the drug and reassess.
Bleomycin. Serial DLCO is how oncologists catch this early, because the lung scars before the marrow ever notices. Falling DLCO plus normal counts equals bleomycin.
Board Walkthrough
Full vignettes with clue highlights. Pick your answer, then walk through every option.
SIX ORIGINAL VIGNETTES
