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42 Cards in this Set

  • Front
  • Back
What is poison?
Any substance which, when introduced into or absorbed by a living organism, destroys life or injures health, irrespective of mechanical means or direct thermal changes.
What is an antidote?
“A medicine given to counteract the influence of poison, or an attack of
Management principles regarding poison?
Identify poison
Monitor & maintain vital signs
(Maintain respiration and circulation – primary
Judge progress of intoxication by: Measuring and charting vital signs and reflexes )
decrease further exposure
decrease further absorption
increase elimination
Specific therapy (specific antidote if available)
Eg. In insecticide poisoning cholinesterase inhibition occurs
Antidotes – Atropine &
Cholinesterase reactivators


Ipecac consists of cephæline, which stimulates the central vomiting centre and _________, which activates sensory receptors in the proximal small intestine
Gastric lavage?
insert tube into stomach and wash stomach with water or ½ normal saline to remove unabsorbed poison
Contraindications are the same as for emesis except that the procedure should not be attempted with young children
Emesis: Contraindications?
ingestion of corrosives such as strong acid or alkali; WHY??P--
if patient is comatose or delirious;
if patient has ingested a CNS stimulant or is convulsing; WHY?—more stimulation?
if patient has ingested a petroleum distillate WHY???
Who am I?

Used for ingestion of enteric coated tablets when time after ingestion is longer than one hour
Use saline cathartics such as sodium or magnesium sulfate
X-ray for location of enteric coated pills and use cathartics if in the stomach
Chemical Adsorption: Activated charcoal

Activated charcoal adsorb on to the charcoal and thereby prevent absorption in the first place .
It may create a ____________, such that drug or metabolite is eliminated faster
concentration gradient across the mesenteric vasculature
Chemical Adsorption: Activated charcoal

Useful for some drugs that undergo substantial enterohepatic recirculation, or small volume of distribution or low protein binding and are highly adsorbed by charcoal
Do not use simultaneously with ________if poison is excreted into bile in active form WHY???
Increasing elimination?
Decreasing passive resorption from nephron lumen
Peritoneal dialysis
If volume of distribution is very large;
do not waste time on any type of dialysis

The heavy metals cause injury by forming _____________and other physiologically important molecules.
complexes with enzymes
The environmental metals of greatest concern are _______________ (4), Other metals responsible for poisoning _______ (3)
lead, mercury, arsenic, and cadmium..

iron, gold & copper
Who am I?

Treatment of arsenic & mercury toxicity.
It is also used with edetate in lead poisoning.
I am more effective in preventing than reversing binding that has already taken place.
Most effective if administered 1-2 hours after metal ingestion.
What are the adverse effects of dimercaprol?
Chelates formed are unstable at acidic pH; metals may dissociate & produce renal metal toxicity if urine is acidic.
Urine should be kept alkaline during therapy.
Transient hypertension, tachycardia,headache, paresthesia
Long term use : thrombocytopenia
Who am I?

Water soluble bidentate congener of dirmercaprol
Commonly used to treat lead poisoning in children (Oral ) and adults
Also binds with high affinity to mercury, and arsenic.
Binding is less avid with copper & zinc.
What are the adverse effects of Succimer?
Nasal congestion, muscle pain, rash.
Teratogenic in animals; contraindicated in pregnant patients.
Who am I?

Used for treatment of lead poisoning.
Because it is very polar, it is given parenterally
To prevent dangerous hypocalcemia, it is usually given as Calcium disodium salts
Calcium EDTA
What are the adverse effects of calcium EDTA?
Renal tubular necrosis; monitor by daily urinalysis.
If renal toxicity develops discontinue use.
Who am I?

For treatment of copper poisoning and Wilson’s Disease.
It is sometimes used as adjunctive therapy in gold, arsenic & lead intoxication and in rheumatoid arthritis
what are the adverse effects of Penicillamine?
Anaphylactic reactions
Bone marrow suppression.
Dermatomyositis, polymyositis, lupus erythematosus, alveolitis, & myasthenia gravis.
Renal toxicity.
Who am I?

I am an antidote for iron poisoning –
it chelates the free iron to form feroxamine, Fortunately, the drug competes poorly for heme iron in haemoglobin and cytochromes
Feroxamine is excreted unchanged in the urine
AE : Skin reactions , longterm use , neurotoxicity (retinal degeneration ), hepatic and renal dysfunction and severe coagulopathies
What are the signs and symptoms of Arsenic (wood preservatives, pesticides, ant poisons)?
Acute: GI distress, garlic breath, "rice water“ stools, torsades, seizures
Chronic: pallor, skin pigmentation, alopecia, stocking glove neuropathy, myelosuppression
What are the intervention/antidotes of Arsenic (wood preservatives, pesticides, ant poisons)?
Activated charcoal, dimercaprol Penicillamine or succimer
what are the signs and symptoms of Iron (medicinal for anemias & prenatal supplements)?
Acute (mainly children): severe GI distress → necrotizing gastroenteritis with hematemesis & bloody diarrhea, dyspnea, shock, coma
what are the intervention/antidotes of Iron (medicinal for anemias & prenatal supplements)?
Gastric aspiration + carbonate lavage, deferoxamine IV
(a.k.a desferrioxamine, desferoxamine)
What are the signs and symptoms of Lead (tap water, leaded paint chips, herbal remedies, gas-sniffing, glazed kitchenware, etc.)?
Acute: N & V, GI distress & pain, malaise, tremor, tinnitus, paresthesias, encephalopathy (red or black feces)
Chronic: multisystem effects-anemia (↓ heme synthesis), neuropathy (wrist drop), nephropathy (proteinuria, failure), hepatitis, mental retardation (from pica), ↓ fertility & ↑ stillbirths
the following is an intervention/antidote for what?

Succimer or Dimercaprol or Calcium EDTA (non specific )
In Children: succimer PO
Lead (tap water, leaded paint chips, herbal remedies, gas-sniffing, glazed kitchenware, etc.)
The following are signs and symptoms of what?

Acute: vapor inhalation – chest pain, dyspnea, pneumonitis
Acute: inorganic salt ingestion – GI distress & bleeding, shock, renal failure
Chronic: organic Hg – CNS effects, ataxia, paresthesias, auditory & visual loss
Mercury (elemental in instruments); salts used in amalgams, batteries, dyes, electroplating, fireworks, photography
The following is the intervention/antidote for what?

Succimer PO or dimercaprol (IM). Activated charcoal for oral ingestion, then support with succimer PO or dimercaprol (NOT IV → causes redistribution of Hg to the CNS → ↑ neurotoxicity
Mercury (elemental in instruments); salts used in amalgams, batteries, dyes, electroplating, fireworks, photography
The following are signs/symptoms of what?

Acute: nausea, vomiting, and diarrhea
Chronic: Hemolytic anemia and anuria
Copper poisoning (Wilson’s Disease).
The following is the intervention/antidote for what?

hemodialysis may be effective if used early.
copper poisoning

It acts as a ____________and so boosts the resynthesis of this vital intracellular agent and thus prevent liver damage or
The ___________ may bind and detoxify the metabolite directly or
NAC may act as an antioxidant and block reactive oxygen species- dependent cell death
If N-acetyl cysteine is given early enough (i.e. within 24 hours) it can reduce mortality dramatically.•
Without intervention, death in 6-25% of individuals; with intervention, death in 1-2%.
precursor for glutathione synthesis ; sulphydryl group of N-acetyl cysteine
Salicylate & Urinary Alkalisation

Ingestion of > 300 mg/kg - serious toxic reactions;
Ingestion of > 500 mg/kg - is potentially fatal.
Poisoning often through suicide (~2% mortality) or chronic ingestion from therapeutic misadventure
Aspirin is readily hydrolysed to salicylate, which stimulates the ___________, producing hyperventilation, respiratory alkalosis and eventually ___________
Produces tinnitus, nausea, vomiting, ataxia, coma and hyperthermia
medullary respiratory centre; metabolic acidosis
Who am i?

is used in the prophylaxis and treatment of venous thrombosis & pulmonary embolism
– it inhibits the synthesis of vitamin K dependent coagulation factors. This results in a sequential depression of Factors II, VII, IX and X activities
__________ are used extensively in agriculture, industrial & occasionally terrorism (sarin)
Toxicity varies markedly
–LD50 > 1000 mg/kg: malathion (Cythion®), phoxim (Baythion®)
–LD50 50 – 1000 mg/kg: chlorpyriphos (Raid®) dichlorvos (Armourcrop®), diazinon (Yates soil insect killer)
–LD50 < 50 mg/kg: methamidophos (Monitor®), Sarin
Organophosphates Diagnosis

GI cramps
Organophosphates Diagnosis

Fasciculation, paralysis, ↑ BP
Organophosphates Diagnosis

head ache, coma, seizure, resp dep
Organophosphates Diagnosis

Serum ChE activity?
10 ml blood, refrigerate, test within 3 wks
Plasma ChE commonly done
If <50% of normal - toxicity
Organophosphates & Pralidoxime

Initially give _______ to antagonize the ACh then Pralidoxime
Pralidoxime can remove __________ to regenerate catalytic activity
– Effects at nicotinic > muscarinic
– Effect is great at erythrocytic esterase if given soon after toxicity
– Reactivation of plasma cholinesterase activity is minimal
Most effective if given < 24 h after organophosphate exposure; phosphorylation becomes _________
Treatment may be required for days depending on the half-life of the toxicant
atropine; phosphate group from the cholinesterase enzyme ; “aged” and irreversible
who am i?

It is an antagonist at the µ, . and d opioid receptors . It may be necessary to administer the drug by i.m., s.c., endotracheal or intralingual routes
it has a shorter half life than heroin, so
relapse may occur