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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.
39 monographs · mechanism, not management · management is TOXBASE and NPIS 0344 892 0111
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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.
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
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
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
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
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
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
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
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
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