Poison And Treatment

Front 1

What is poison?

Back 1

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.

Front 2

What is an antidote?

Back 2

“A medicine given to counteract the influence of poison, or an attack of
disease.”

Front 3

Management principles regarding poison?

Back 3

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

Front 4

PREVENTION OF ABSORPTION OF POISON

Emesis:

Ipecac consists of cephæline, which stimulates the central vomiting centre and _________, which activates sensory receptors in the proximal small intestine

Back 4

emetine

Front 5

Gastric lavage?

Back 5

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

Front 6

Emesis: Contraindications?

Back 6

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???

Front 7

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

Back 7

purgation

Front 8

PREVENTION OF ABSORPTION OF POISON
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

Back 8

concentration gradient across the mesenteric vasculature

Front 9

PREVENTION OF ABSORPTION OF POISON
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???

Back 9

ipecac

Front 10

Increasing elimination?

Back 10

Decreasing passive resorption from nephron lumen
Diuresis
Cathartics
Peritoneal dialysis
Hemodialysis
Hemoperfusion

Front 11

If volume of distribution is very large;
_____________________________

Back 11

do not waste time on any type of dialysis

Front 12

HEAVY METAL CHELATORS

The heavy metals cause injury by forming _____________and other physiologically important molecules.

Back 12

complexes with enzymes

Front 13

The environmental metals of greatest concern are _______________ (4), Other metals responsible for poisoning _______ (3)

Back 13

lead, mercury, arsenic, and cadmium..

iron, gold & copper

Front 14

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.

Back 14

Dimercaprol

Front 15

What are the adverse effects of dimercaprol?

Back 15

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

Front 16

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.

Back 16

Succimer

Front 17

What are the adverse effects of Succimer?

Back 17

Nasal congestion, muscle pain, rash.
Hepatotoxic.
Teratogenic in animals; contraindicated in pregnant patients.

Front 18

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

Back 18

Calcium EDTA

Front 19

What are the adverse effects of calcium EDTA?

Back 19

Renal tubular necrosis; monitor by daily urinalysis.
If renal toxicity develops discontinue use.

Front 20

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

Back 20

Penicillamine

Front 21

what are the adverse effects of Penicillamine?

Back 21

Anaphylactic reactions
Bone marrow suppression.
Dermatomyositis, polymyositis, lupus erythematosus, alveolitis, & myasthenia gravis.
Renal toxicity.

Front 22

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

Back 22

Deferoxamine

Front 23

What are the signs and symptoms of Arsenic (wood preservatives, pesticides, ant poisons)?

Back 23

Acute: GI distress, garlic breath, "rice water“ stools, torsades, seizures
Chronic: pallor, skin pigmentation, alopecia, stocking glove neuropathy, myelosuppression

Front 24

What are the intervention/antidotes of Arsenic (wood preservatives, pesticides, ant poisons)?

Back 24

Activated charcoal, dimercaprol Penicillamine or succimer

Front 25

what are the signs and symptoms of Iron (medicinal for anemias & prenatal supplements)?

Back 25

Acute (mainly children): severe GI distress → necrotizing gastroenteritis with hematemesis & bloody diarrhea, dyspnea, shock, coma

Front 26

what are the intervention/antidotes of Iron (medicinal for anemias & prenatal supplements)?

Back 26

Gastric aspiration + carbonate lavage, deferoxamine IV
(a.k.a desferrioxamine, desferoxamine)

Front 27

What are the signs and symptoms of Lead (tap water, leaded paint chips, herbal remedies, gas-sniffing, glazed kitchenware, etc.)?

Back 27

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

Front 28

the following is an intervention/antidote for what?

Succimer or Dimercaprol or Calcium EDTA (non specific )
In Children: succimer PO

Back 28

Lead (tap water, leaded paint chips, herbal remedies, gas-sniffing, glazed kitchenware, etc.)

Front 29

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

Back 29

Mercury (elemental in instruments); salts used in amalgams, batteries, dyes, electroplating, fireworks, photography

Front 30

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

Back 30

Mercury (elemental in instruments); salts used in amalgams, batteries, dyes, electroplating, fireworks, photography

Front 31

The following are signs/symptoms of what?

Acute: nausea, vomiting, and diarrhea
Chronic: Hemolytic anemia and anuria

Back 31

Copper poisoning (Wilson’s Disease).

Front 32

The following is the intervention/antidote for what?

Penicillamine
hemodialysis may be effective if used early.

Back 32

copper poisoning

Front 33

The MOA of N-ACETYL CYSTEINE

MOA :
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%.

Back 33

precursor for glutathione synthesis ; sulphydryl group of N-acetyl cysteine

Front 34

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

Back 34

medullary respiratory centre; metabolic acidosis

Front 35

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

Back 35

Warfarin

Front 36

__________ 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

Back 36

Organophosphates

Front 37

Organophosphates Diagnosis

Muscarinic?

Back 37

Salivation
Lacrimation
Urination
Defecation
GI cramps
Emesis

Front 38

Organophosphates Diagnosis

Nicotinic

Back 38

Fasciculation, paralysis, ↑ BP

Front 39

Organophosphates Diagnosis

CNS

Back 39

head ache, coma, seizure, resp dep

Front 40

Organophosphates Diagnosis

Serum ChE activity?

Back 40

10 ml blood, refrigerate, test within 3 wks
Plasma ChE commonly done
If <50% of normal - toxicity

Front 41

Organophosphates & Pralidoxime

Antidote
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

Back 41

atropine; phosphate group from the cholinesterase enzyme ; “aged” and irreversible

Front 42

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

Back 42

Naloxone