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Toxicology Monographs
Referenced articles on what a poison is actually doing inside someone, and when. What the toxic species is — usually not the thing they swallowed — how it is made, which organ it destroys and why that organ, and how the whole thing unfolds against the clock.
A poison is a drug whose kinetics have escaped its pharmacology.
72 monographs · mechanism, not management · management is TOXBASE and NPIS 0344 892 0111
A
Botanical cardiotoxin — the sodium channel held open, the mirror image of blockade
Aconite (aconitine)
Monkshood produces the mirror image of the yew and local-anaesthetic lesion: instead of blocking the sodium channel it stops it closing, so the channel fires and re-fires. The result is a tingling face, a poisoned nervous system and a refractory ventricular arrhythmia — with no antidote to reverse it.
Oral and limb paraesthesia within minutes to an hour, then ventricular arrhythmia over hours
The UK's only native venomous bite — a local injury that occasionally turns systemic
Adder envenomation (Vipera berus)
The only venomous snake native to Britain injects a protein venom whose zinc metalloproteinases tear open the vasculature of a limb — producing dramatic swelling that looks surgical and almost never is. In about a third of cases the venom turns systemic, with an early anaphylaxis-like collapse that is the real emergency.
Immediate local pain and swelling that spreads over hours; an early systemic reaction in about a third
Stimulant — releasers rather than reuptake blockers, and the difference matters
Amphetamines and MDMA
Cocaine blocks the door; amphetamines run it backwards. Reverse transport has no ceiling, and the two consequences that kill are the two a stimulant is least expected to produce: hyperthermia, and hyponatraemia.
Hours of sympathomimetic drive, then the two things that kill: heat, and sodium
Four poisons that produce one sign, and answers that do not interchange
Anticoagulants
The clearest demonstration in the library that an antidote answers a mechanism rather than a syndrome. Several anticoagulants produce one clinical sign and a set of answers that do not interchange — and only the vitamin K antagonists among them have a latent phase.
The direct inhibitors bleed today; warfarin bleeds the day after tomorrow
A class named after the receptor that causes the least trouble
Antihistamines
A class defined by a receptor whose blockade is close to harmless. What poisons is everything else these molecules do — muscarinic blockade, sodium-channel blockade and delayed repolarisation — and whether they can reach the brain at all.
Sedation or agitation within hours; the ECG is what decides how serious it is
Neuroleptic — three drugs, three overdoses, one receptor in common
Antipsychotics
Three drugs sharing one receptor and almost nothing else in overdose. What unites them is a warning printed on all three UK labels: do not give adrenaline, because alpha blockade turns a vasopressor into a vasodilator.
Sedation and tachycardia early, QT and seizures later, and a bezoar that changes everything
Metalloid — two oxidation states with two unrelated mechanisms, and a mechanism its own literature says is not settled
Arsenic
One element in two oxidation states, poisoning by two unrelated chemistries — arsenate substituting for phosphate in energy metabolism, arsenite binding the thiols that enzymes depend on. The account is coherent, widely taught, and described in the peer-reviewed literature as not established.
Vomiting and shock in hours · multi-organ within a day · a neuropathy and white nail lines weeks later
Gas — the same element as arsenic, and almost nothing on the arsenic page applies
Arsine and stibine
An industrial gas that is chemically arsenic and toxicologically nothing like it. Arsine targets the erythrocyte and causes intravascular haemolysis; the renal failure that follows the haemolysis is what kills, and chelation does not address either.
Non-specific symptoms in hours · haemoglobinuria at 4–6 h · jaundice at 1–2 days · anuria within two
B
A drug that barely reaches its own target by mouth, and kills when the route is fixed
Baclofen
A GABA-B agonist whose entire clinical story is decided by the route it is given by. Oral overdose looks alarming and usually recovers; abrupt loss of an intrathecal infusion produces a hypermetabolic syndrome that has killed.
Hours to full effect, days to recovery, and a withdrawal syndrome that is the dangerous half
Sedative — the poison with a pharmacological ceiling
Benzodiazepines
A poison defined by what it cannot do. The ceiling that makes benzodiazepines safe alone is the same property that makes the combination dangerous.
Sedation without hypoventilation · the risk is what else was taken
Beta-adrenoceptor antagonists — three different poisons sharing a receptor
Beta-blockers
The receptor they share is the least useful thing about them. Lipid solubility, protein binding and a second channel target make propranolol, sotalol and atenolol three separate poisonings with one name.
Bradycardia and hypotension — but propranolol seizes and sotalol torsades
Not a systemic poison — a chemical burn delivered from inside
Button batteries and caustics
Neither of these is a poison in the sense of the rest of the library — nothing is absorbed to act at a distant target. The damage is a chemical burn delivered to whatever tissue the agent touches. For a button battery the burn is generated electrically, and it starts within two hours; for caustics it is instantaneous. The mechanism dictates a race against the clock and a short list of things not to do.
Button battery: severe tissue injury within 2 hours. Caustics: burn on contact, with delayed stricture over weeks
C
The world's most-taken drug, and in overdose the theophylline story — a β-adrenergic storm with a low potassium
Caffeine
A methylxanthine central stimulant, taken daily by most of the world and lethal in gram quantities. In overdose it reproduces the toxicology of theophylline: adenosine antagonism and massive catecholamine release drive a β-adrenergic storm — tachyarrhythmia, hypokalaemia, hyperglycaemia, lactic acidosis, tremor and seizures — that supportive care, β-blockade and, in severe cases, extracorporeal removal are aimed at.
A caffeinated normal life, a purchasable overdose in powder form, and a β-adrenergic storm that reads like theophylline — tachyarrhythmia, hypokalaemia, seizures
L-type channel antagonists — the poison that starves the heart of fuel
Calcium-channel blockers
The same L-type channel sits on the myocyte, the vessel wall and the pancreatic beta cell. Block all three and you produce a shocked patient who cannot release insulin — which is why the glucose rises, and why insulin is a treatment.
Hyperglycaemia early; modified-release absorption may run beyond 48 hours
Agricultural insecticide — the same enzyme, inhibited reversibly, and not the milder illness that predicts
Carbamate insecticides
Carbamates make the same lesion as organophosphates in a form that undoes itself. No bioactivation, no aging, no intermediate syndrome, and no need for an oxime. The chemistry predicts a benign illness and the outcome data decline to agree.
The same cholinergic crisis, arriving sooner and ending sooner — and then no second act
Antiepileptic — a tricyclic-shaped molecule that blocks sodium channels and slows its own absorption
Carbamazepine
A tricyclic-shaped anticonvulsant that poisons in three registers at once — cerebellar, anticholinergic and sodium-channel — and then hides more of itself in a gut its own antimuscarinic effect has slowed. The relapse on day two is the signature.
Ataxia and anticholinergic signs first · a widening QRS and fluctuating consciousness · relapse on day two or three as a gut reservoir releases more drug
Confined-space gases — the category the rest of this band is defined against
Carbon dioxide and the simple asphyxiants
The only entries in this library that are not poisons. A true simple asphyxiant does nothing to the body at all — it occupies the space oxygen would have filled. Carbon dioxide is the impostor in the category: it displaces oxygen and is pharmacologically active, which is why it is the one asphyxiant that warns you.
Carbon dioxide announces itself with air hunger; an inert gas does not announce itself at all
Gas — cellular asphyxiant with a delayed neurological second act
Carbon monoxide
The poison whose measurable marker is the least useful thing about it. Carbon monoxide's second injury begins after the gas has gone.
Non-specific acutely · delayed neurological sequelae days to weeks later
Irritant gases — where the injury lands is decided by how readily the gas dissolves
Chlorine and ammonia
Two irritant gases, one variable. Ammonia is extremely water-soluble and is almost entirely retained in the upper nasal mucosa, which protects the lungs and produces immediate agonising symptoms. Chlorine is less soluble, so it travels further before it reacts — and the injury it causes may not declare for a day and a half.
Ammonia hurts at once and stops at the top until the dose overwhelms it; chlorine hurts less, goes deeper, and either gas can flood the lungs a day and a half later
4-aminoquinoline antimalarials — the rapidly-lethal cardiotoxins that a trial taught us to treat by sedating and supporting, not removing
Chloroquine and hydroxychloroquine
The antimalarials that can stop the heart within hours. Chloroquine and hydroxychloroquine are membrane-stabilising sodium-channel blockers whose overdose brings rapid hypotension, a wide QRS and cardiac arrest, with a hypokalaemia that is a shift not a deficit. Dialysis cannot touch them; a trial showed survival improved with early ventilation, diazepam and adrenaline.
Little warning · then rapid cardiovascular collapse — hypotension, wide QRS, arrhythmia and cardiac arrest — with hypokalaemia and seizures
Sympatholytic — the poison that impersonates an opioid
Clonidine and central α₂ agonists
Miosis, coma, bradycardia and apnoea — the opioid toxidrome produced without an opioid. The label even suggests naloxone. Whether that works, and why, is less settled than the teaching suggests.
Looks like opioid poisoning; may be hypertensive first and small doses matter in children
Stimulant — a local anaesthetic that reached the whole body
Cocaine
Cocaine is a local anaesthetic that escaped the nose. Its sympathomimetic effects are the famous half; its sodium-channel blockade — a wide QRS treated with bicarbonate — is the half that is forgotten until the ECG is printed.
Minutes to peak, an hour of danger, and a molecule that is three poisons at once
Antimitotic alkaloid — the narrow-window poison whose worst phase arrives after the patient looks better
Colchicine
The overdose that looks like gastroenteritis before it kills. Colchicine arrests cell division in the tissues that divide fastest, so a vomiting, crampy first phase can appear to settle — and then, at 24–72 hours, the marrow, the heart, the kidneys and the nerves fail together. There is no antidote and dialysis does not work.
A gastrointestinal first phase · a deceptive lull · then multi-organ failure and marrow collapse at 24–72 hours
Industrial chemical and combustion product — the poison that stops the last step of respiration
Cyanide
Oxygen delivery is normal, oxygen extraction is not. Cyanide binds the ferric iron of cytochrome c oxidase, the electron transport chain stops at its final step, and every cell switches to anaerobic metabolism at once. The saturation probe reports success while the mitochondria fail.
Seconds to minutes from a lethal concentration; no latent phase, and the lactate rises before anything else does
D
Amatoxin — the library's purest latent-phase poison, and its clearest case for early treatment
Death cap and the amatoxin mushrooms
The death cap is the botanical answer to paracetamol: a poison whose danger lives entirely in its latency. By the time the liver declares itself, the transcription machinery has been shut down for two days. The one lever that works — blocking hepatocyte uptake — only works before the uptake has happened.
A deceptively long latent phase (6–40 h), a gastrointestinal phase, apparent recovery, then hepatic failure from day 3
Cardiac glycoside — the poison that is mostly not in the blood
Digoxin
A poison with a 510-litre volume of distribution and a receptor on every cell in the body. The blood concentration is the one place the poison mostly is not — which defeats the level, the dialyser, and some of the intuition about the antidote.
Vomiting first, cardiac peak at 3–6 h, arrhythmia for a day or more
E
Alcohol — sedative, and the reference poison for saturation kinetics
Ethanol
The most familiar poison in the department, and the one whose most-quoted number does not survive contact with its own biochemistry.
No latent phase · the danger is what else is happening
Toxic alcohol — poisoning by metabolite, not by parent
Ethylene glycol
Antifreeze is barely toxic. Everything that harms the patient is made after they swallow it — which is why the antidote is an enzyme blocker and why waiting for symptoms is the error.
Inebriation 0–3 h · latent 3–12 h · acidosis 12–24 h · AKI 24–72 h
F
Botanical cardiac glycoside — digoxin's mechanism, without digoxin's assay
Foxglove and the cardiac-glycoside plants
The plants that give us digoxin also give us its poisoning, at the same pump — but with two differences that decide the resus: the laboratory assay is calibrated for the wrong molecule and reads them unreliably, and the antidote cross-reacts and works anyway.
Vomiting early, cardiac toxicity over hours, arrhythmia persisting a day or more
G
Sedative — a coma that ends as abruptly as it began
GHB and GBL
The library's shortest poisoning and its steepest. Sodium oxybate's own UK label records that doubling the dose from 4.5 g to 9 g increases exposure 3.8-fold — which is why the margin between a recreational dose and a coma is so narrow.
Deep coma within 15 minutes, gone within a few hours, and nothing reverses it
Two drugs that share a target and disagree about almost everything else
Gabapentinoids
A poison that is mostly harmless alone and repeatedly lethal in company. The gabapentinoid label carries the odds ratio for its own contribution to opioid death, and EXTRIP's recommendation turns entirely on whether the kidneys work.
Fast in, slowly out if the kidneys are gone; the danger is nearly always what was taken with it
H
Two different plants, two different lesions, one dangerous name
Hemlock — poison hemlock and water hemlock
One English word covers two unrelated poisons. Poison hemlock kills like a depolarising muscle relaxant — ascending paralysis and respiratory failure. Water hemlock kills by tearing the brakes off the brain — refractory status epilepticus. Getting the two the same because they share a name is the error the page exists to prevent.
Water hemlock: violent seizures within an hour. Poison hemlock: nicotinic effects then ascending paralysis over hours
Industrial and domestic acid — a burn that hurts later, goes deeper, and kills by the ion rather than the wound
Hydrofluoric acid
Two poisons in one liquid. The hydrogen ion burns like any acid and stops at the surface. The fluoride ion keeps going — through intact skin, into deep tissue and bone — precipitating the calcium and magnesium the heart needs.
A burn that may not hurt for a day, and a cardiac arrest that arrives before the skin looks bad
Industrial and confined-space gas — a signalling molecule the body makes, at a concentration that stops the brainstem
Hydrogen sulphide
The body makes this gas on purpose and uses it to signal. Inhaled at industrial concentrations it inhibits the same enzyme as cyanide, and it is taken up more by the brainstem than by anything else — which is why the first sign is often collapse and the second is apnoea.
A warning smell that stops working, then collapse in a breath or two — and often complete recovery if the exposure is ended
I
The hormone that is an antidote two pages over, and a poison here — a therapeutic action given without its off-switch
Insulin
The injected hormone in excess. Insulin poisoning is a single, prolonged catastrophe — hypoglycaemia deep enough to deprive the brain of its obligate fuel, accompanied by hypokalaemia as potassium follows glucose into cells. It is treated by replacing what the hormone consumes: glucose, sometimes for days, because a long-acting depot can outlast any single correction.
A hormone dosed without its counter-regulatory brake, a long-acting depot that starves the brain for days, and a treatment measured in litres of glucose over two days or more
Metal — an overdose of a nutrient, and the only poison here the body has no route to excrete
Iron
An overdose of a nutrient with no excretory pathway. Transferrin saturates, free iron appears, and the poisoning proceeds in four phases — the second of which is a genuine remission that has fooled clinicians into discharging patients.
Corrosive hours 0–6 · a genuine remission 6–24 h · shock and liver from about 12 h · a stricture at 2–5 weeks
Antituberculous hydrazide — the seizure that will not stop until you replace a vitamin
Isoniazid
The overdose whose seizures will not stop on benzodiazepines alone, because the problem is a missing vitamin. Isoniazid depletes the active form of vitamin B6, the cofactor the brain needs to make GABA — so the classic triad is refractory seizures, a lactic acidosis and coma, and the antidote is pyridoxine.
A short quiet gap after ingestion · then the triad — refractory seizures, a high-anion-gap lactic acidosis and coma — arriving together and fast
The toxic alcohol that isn't — an osmolar gap with no acidosis, because its metabolite is a ketone, not an acid
Isopropanol
A household and hospital alcohol — rubbing alcohol, hand sanitiser — twice as CNS-depressant as ethanol and metabolised by alcohol dehydrogenase to acetone. Because acetone is a ketone and not an organic acid, isopropanol is the toxic alcohol that produces an osmolar gap without a metabolic acidosis, has no latent phase, and needs no enzyme blockade.
The toxic alcohol with no latent phase and no killing acidosis — drunk faster than ethanol, cleared without a poison, dangerous only when it is deep enough to stop the circulation
K
Dissociative anaesthetic — the drug whose acute safety is the reason its chronic harm was missed
Ketamine
Ketamine's label states that unintentional administration of up to ten times the usual dose has been followed by prolonged but complete recovery. Almost no drug in this library can say that. The harm moved somewhere the acute presentation never looks: the bladder.
An hour of dissociation with a wide acute margin, and a bladder destroyed over years
L
The plant whose reputation exceeds its poisoning — a nicotinic agonist now sold as medicine
Laburnum (cytisine)
Laburnum has one of the most alarming reputations of any garden plant and one of the mildest usual courses. Its toxin, cytisine, is a nicotinic agonist — the same molecule now licensed as a smoking-cessation aid — and most childhood ingestions produce little more than vomiting. The mechanism explains both the fear and the reality.
Nausea and vomiting within an hour or two; serious nicotinic features only after large ingestions
A sodium-channel blocker given on purpose — therapeutic in the neurone, cardiotoxic in the myocardium, and convulsant in overdose
Lamotrigine
A voltage-gated sodium-channel blocker used as an anticonvulsant and mood stabiliser. In overdose it produces the two things its mechanism predicts once the dose is high enough — cardiac conduction delay of the sodium-channel-blockade type, and, paradoxically, generalised seizures — and its long half-life makes both persist.
An anticonvulsant that causes convulsions, a sodium-channel drug that widens the QRS, and a 33-hour half-life that makes both last
Metal — a poison whose critical effects have no demonstrated threshold, measured in the compartment that holds least of it
Lead
Lead is handled by the body as a counterfeit calcium — absorbed on calcium's transporters, stored in bone as an insoluble phosphate, and released again whenever the skeleton is resorbed. Its most sensitive effects have no demonstrated threshold, and the test used to measure it samples the compartment holding about five per cent of it.
Weeks to decades — and a blood concentration that can rise years after the exposure stopped
An ion, not a drug — the only poison in the band EXTRIP grades dialysable at level of evidence A
Lithium
The only poison in Band B that dialyses perfectly — an unbound, unmetabolised ion in a small volume of distribution. And the one where removing the poison fastest does the least to make the patient better soonest.
The concentration falls fast and the patient improves slowly — they are different curves
The sodium-channel blocker injected on purpose — and the one poisoning in the library with a purpose-built antidote
Local anaesthetic systemic toxicity (LAST)
The systemic toxicity of local anaesthetic drugs when they reach the circulation in excess — from inadvertent intravascular injection or absorption of a large dose. It is sodium-channel blockade produced on purpose in a nerve and by accident in the brain and heart, running from CNS excitation and seizures to a bupivacaine cardiac arrest, and it is the one poisoning in this library with an antidote designed specifically for it: intravenous lipid emulsion.
A tingling lip that becomes a seizure that becomes an arrest — sometimes at the needle, sometimes an hour later from a slowly absorbed depot, and the one syndrome here with an antidote made for it
M
Metal — one element, three poisonings, and the route of exposure decides which one the patient gets
Mercury
The same element produces three different illnesses depending on how it is met. Swallowed liquid metal is barely absorbed at all; the same metal as vapour crosses the alveolus, crosses the blood-brain barrier, and is then oxidised into an ion that does not readily cross back out.
Vapour: pneumonitis in hours, brain in days, tremor over weeks. Swallowed liquid metal: essentially nothing.
Biguanide antihyperglycaemic — the overdose whose danger is an acidosis, not a hypoglycaemia
Metformin
The antidiabetic that does not cause hypoglycaemia in overdose. Metformin's danger is a lactic acidosis, not a low sugar — it inhibits mitochondrial respiration and lets lactate accumulate, and the patient who dies is the one whose pH falls while the glucose stays normal.
Gastrointestinal upset early · a widening lactic acidosis underneath · shock, coma and renal failure if the acidosis is not reversed
Industrial and pharmaceutical oxidants — the poisoning that is defined by an oxidation state rather than by a molecule
Methaemoglobin inducers
One electron, one iron atom, and haemoglobin stops working. Methaemoglobin forms when ferrous iron is oxidised to ferric, which cannot bind oxygen — so the blood is full, the lungs are fine, and the tissues are starved.
Cyanosis one to four hours after exposure, in a patient whose saturations will not improve on oxygen
Toxic alcohol — poisoning by metabolite, with a single-organ signature
Methanol
One carbon smaller than ethanol and a completely different disease. Methanol is the library's clearest demonstration that the metabolite, not the parent, chooses the target organ.
Drunk at 4 h · quiet 10–12 h · acidosis and blindness 12–48 h
Antifolate antimetabolite — the overdose that starves dividing cells of folate, and is often a weekly drug taken daily
Methotrexate
The antifolate whose commonest poisoning is a dosing error — a weekly drug taken daily. Methotrexate blocks the enzyme that regenerates active folate, so the fastest-dividing tissues fail over days. Folinic acid bypasses the block to rescue normal cells; glucarpidase, not dialysis, removes the drug; and alkalinising the urine stops it precipitating in the kidney.
Little early · then, over days, the antifolate injury — mucositis, marrow failure, renal injury — declaring in the fastest-dividing tissues
N
Non-steroidal anti-inflammatory drugs — the common overdose that is usually benign, and the dose at which that stops being true
NSAIDs
The overdose that is usually nothing — until it is not. Most NSAID ingestions cause little more than nausea and drowsiness, because reversible COX inhibition is forgiving; but a massive dose adds a metabolic acidosis, seizures and renal injury within hours, and mefenamic acid causes seizures at more modest doses. There is no antidote.
Usually little or nothing · GI upset and drowsiness when symptomatic · and in massive overdose an acidosis, seizures and renal injury within hours
The alkaloid that stimulates every cholinergic synapse and then blocks it — one receptor, a biphasic poisoning, and a lethal dose that was always a myth
Nicotine
A plant alkaloid and the active drug of tobacco, nicotine replacement and vaping liquids. It is an agonist at nicotinic acetylcholine receptors that, at high dose, depolarises and then blocks them — producing a biphasic poisoning of early cholinergic and adrenergic overstimulation followed by ganglionic and neuromuscular blockade, flaccid paralysis and respiratory failure.
A receptor that excites and then blocks, a biphasic course from adrenergic storm to flaccid paralysis, and a famous lethal dose that turned out to be a nineteenth-century guess
Inhaled gas — the poison that works by oxidising a metal atom
Nitrous oxide
The only poison in this library whose target is a single metal atom. Nitrous oxide oxidises the cobalt of vitamin B12 from Co(I) to Co(III), and methionine synthase — which needs it in the reduced state — stops. Nothing happens for weeks. Then the spinal cord fails.
Minutes of euphoria, then weeks to months of silence, then a myelopathy that may not fully recover
O
Analgesic — respiratory depression by receptor occupancy
Opioids
The only Band A poison whose antidote is given to reverse something that is actively killing the patient — and the one where that antidote's own kinetics create the next problem.
Minutes to hours · renarcotisation is the risk after reversal
Agricultural insecticide — the poison that makes an enzyme permanently the wrong shape
Organophosphate insecticides
Two chemical events decide everything. First the liver turns a weak inhibitor into a potent one. Then the inhibited enzyme loses an alkyl group and becomes permanently the wrong shape — after which no antidote can rebuild it, and the body must synthesise new enzyme instead.
Minutes to hours of a cholinergic crisis, then — after it settles — a second, separate paralysis that takes the diaphragm
P
Analgesic — hepatotoxicity by reactive metabolite
Paracetamol
The commonest deliberate overdose in the UK, and the one where the poison is not the drug. Paracetamol is harmless until a minor metabolic pathway becomes the major one.
Latent for 24 h · transaminases from ~24 h · peak injury 72–96 h
Herbicide — the poison that is concentrated by the organ it destroys, and uses oxygen to do it
Paraquat
A catalyst rather than a poison. Paraquat takes an electron from NADPH, gives it to oxygen, and returns unchanged to do it again — so one molecule can generate reactive oxygen indefinitely. The lung concentrates it against a gradient, and the lung is where the patient dies.
A burnt mouth, then a few well days, then a lung that fibroses shut
Antiepileptic — the library's second worked example of saturation kinetics, and a poison whose danger is set by the route
Phenytoin
The antiepileptic that clears by a saturable enzyme, so that dose and concentration come apart. Its oral overdose is one of the more benign in the library; its intravenous cardiotoxicity is one of the more feared — and the difference is entirely the route.
Nystagmus, then ataxia, then dysarthria and drowsiness — a concentration-ordered march that seldom reaches the heart when the drug is swallowed
Q
Cinchona antimalarial — the overdose that blinds and blocks the heart, and is made worse by removal
Quinine
The antimalarial that can take the sight and stop the heart. Quinine causes cinchonism and, in serious overdose, irreversible visual loss and a sodium-channel cardiotoxicity that widens the QRS and prolongs the QT — with hypoglycaemia underneath. Multiple-dose charcoal helps; dialysis does not, and EXTRIP recommends against it.
Cinchonism early — tinnitus, deafness, blurred vision · then cardiotoxicity and visual loss · with hypoglycaemia and hypokalaemia underneath
S
Antidepressant — a safe drug whose danger is combinatorial
SSRIs and serotonin toxicity
A class designed to be survivable in overdose, and largely is. What kills is not the SSRI alone but the second serotonergic drug — and the thing to examine for is not confusion or fever but clonus.
Usually a mild overdose; the risk is the interaction, the QT, and the seizure at 6–12 hours
Analgesic — the library's worked example of saturation kinetics
Salicylate
The poison that is its own metabolite. Everything dangerous about salicylate follows from three simultaneous kinetic failures — and from the fact that pH decides where the drug goes.
Alkalosis first · mixed picture · acidaemia is the terminal step
A syndrome, not a drug — one lesion reached from a dozen starting molecules
Sodium-channel blockade
The only entry in this library defined by a channel rather than a molecule. Half a dozen unrelated drugs produce one recognisable ECG, and the treatment is aimed at the channel, not at any of them.
The QRS is the clock; flecainide's half-life means support is measured in days
Insulin secretagogues — the overdose that starves the brain of glucose, for far longer than you expect
Sulfonylureas
The overdose that makes the patient poison themselves with their own insulin. A sulfonylurea keeps the pancreas releasing insulin, so the hypoglycaemia is delayed, recurrent and resistant to glucose alone — and octreotide, which switches the insulin off, is the antidote that fits.
Hypoglycaemia that may be delayed · recurs after every glucose correction · and outlasts a short admission if the drug is long-acting
Designer drug — the same receptor as cannabis, and full agonism at it
Synthetic cannabinoids
Not strong cannabis. THC is a partial agonist at the CB1 receptor and the synthetic compounds are full agonists, which is a difference in kind rather than in dose — and it is why a drug marketed as a cannabis substitute produces seizures and collapse that cannabis does not.
Minutes to a syndrome cannabis does not produce, with a compound nobody can name
T
Metal — mistaken for potassium at every membrane in the body, and the one metal whose metal antidotes are contraindicated
Thallium
Thallium is admitted to every cell in the body because its charge and ionic radius resemble potassium's closely enough to fool the transporters that move it. It is the only metal here with an EXTRIP recommendation, the only one whose standard chelators are contraindicated, and one of the few whose nerve injury outlasts the poison by a year.
Painful ascending sensory neuropathy first, alopecia after it, and a nerve that does not fully recover at a year
A syndrome defined by a receptor that is not being reached
The anticholinergic toxidrome
The library's third entry defined by a lesion rather than a molecule. One receptor block, reached from a dozen unrelated drug classes, and a syndrome whose two halves are separated by whether the molecule carries a permanent charge.
Hours to onset, and a delirium that the labels measure in days rather than hours
Methylxanthine bronchodilator — a narrow therapeutic index and a catecholamine storm
Theophylline
A drug with almost no margin, whose overdose is a self-inflicted phaeochromocytoma. Everything dangerous about theophylline follows from two linked mechanisms — adenosine blockade and a flood of endogenous catecholamines — and from the fact that the sickest patients often have the lowest numbers.
Vomiting and tremor first · a rising concentration behind a prolonged-release shell · seizures and dysrhythmia last
Analgesic — two poisonings in one molecule, and an antidote that treats only one
Tramadol
One tablet, two poisonings. The opioid half depends on a metabolite the patient may or may not be able to make; the serotonergic and seizure half is the parent drug and is untouched by naloxone. The label says so explicitly.
Opioid features naloxone fixes, plus seizures and serotonin toxicity it does not
Antidepressant — sodium-channel blockade as the lethal mechanism
Tricyclic antidepressants
The Band A poison that kills fastest, has no antidote, and cannot be removed. Everything useful comes from one ECG and one pH.
Deteriorates fast · QRS is the clock · risk front-loaded to 6 h
V
Antiepileptic and mood stabiliser — the saturation poison that also depletes a cofactor
Valproate
The saturation poison with a metabolic tail. Most of an overdose is sedating and self-limiting — but valproate also depletes carnitine and drives the urea cycle backwards, so the dangerous patient is the one whose ammonia and encephalopathy arrive after the drowsiness.
Drowsiness and vomiting first · a metabolic acidosis and a rising ammonia underneath · encephalopathy and cerebral oedema that can lag the ingestion
The antidepressant whose overdose the SSRI page cannot explain — because the danger is a seizure, not a serotonin syndrome
Venlafaxine and the SNRIs
A serotonin-noradrenaline reuptake inhibitor whose overdose is defined by a dose-dependent risk of generalised seizures rather than by serotonin toxicity, and whose cardiac reputation rests on label warnings the large prospective cohorts do not reproduce. Its active metabolite, desvenlafaxine, is itself a marketed antidepressant.
Seizures within hours and dose-dependent, an active metabolite that outlives the parent, and a cardiac reputation larger than the cohorts support
Y
Botanical cardiotoxin — a cardiac-glycoside look-alike that the glycoside antidote cannot touch
Yew (taxine alkaloids)
A garden hedge that produces one of the most lethal plant poisonings in the UK by a mechanism that is the opposite of the plant it resembles: taxines block cardiac sodium and calcium channels rather than inhibiting the sodium pump, so the poisoning looks glycoside-like and the glycoside antidote is useless.
Vague early symptoms, then sudden wide-complex bradyarrhythmia and collapse hours after ingestion
Z
The non-benzodiazepines that share the benzodiazepine ceiling at the receptor — and lose it at the mortuary
Z-drugs (zopiclone and zolpidem)
Non-benzodiazepine hypnotics that act as positive modulators at the benzodiazepine site of the GABA-A receptor. Single-agent overdose is usually benign, limited by the same ceiling that protects benzodiazepine overdose; the danger is co-ingestion, and the population death rate is far higher than the receptor pharmacology alone would suggest.
A benign single-agent overdose with a receptor ceiling, a nine-fold higher death rate than diazepam in the population, and a reversal agent the label warns against using
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