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Sign, Sypmtoms and Tretment of Posioning

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SIGN,SYPMTOMS AND

TRETMENT OF POSIONING
SUBMITTED TO: Dr. ZAFAR IQBAL
SUBMITTED BY: GROUP E
 Toxicology is a branch of science that deals with
toxins, poisons, their effects and treatment.
 It is very important for the development of new
drugs and for the extension of the therapeutic
potential of existing molecules.
 Toxicology uses the power of science to predict
what, and how chemicals may cause harm and
then shares that information to protect public
health
A toxic agent is anything that TOXICOLOGICAL AGENGT
can produce an adverse
biological effect. It may be
chemical, physical, or
biological in form. For
example, toxic agents may
be
 chemical (such as
cyanide)
 physical (such as
radiation)
 biological (such as snake
venom
Clinical toxicology: It is mainly involved in
the study of diagnosis and treatment of
poisoning that can occur in humans

For thousands of years, poisons and the study of them


(toxicology) have been woven into the rich fabric of the
human experience.
 Homer and Aristotle described the poison arrow
 Socrates was executed with poison hemlock
 Cleopatra used an African Cobra to commit suicide
 lead poisoning may have helped bring down the
Roman Empire
 Marilyn Monroe, Elvis Presley, and actor Heath
Ledger all fatally overdosed on prescription
medication
WHAT IS POISON
All substances are poisons; there is none which is not a
poison. The right dose differentiate a poison and a remedy”
- Paracelsus (Grand Father of Toxicology)
 Toxins can be inhaled, insufflated (snorted), orally ingested,
injected, and absorbed dermally
 Once in the body, some of the common targets of toxicity
include the central nervous system, the lungs, the kidney, the
heart, the liver, the blood, and even the intricate acid/base
and electrolyte balance of the body
1:ALCOHOL POISONING

 Methanol is found in such


products as windshield
washer fluid and model
airplane fuel.
 Ethylene glycol is most
commonly found in radiator
antifreeze. These primary
alcohols are themselves
relatively nontoxic and cause
mainly CNS sedation.
TOXICITY

However, methanol and


ethylene glycol are oxidized
to toxic products: formic
acid in the case of methanol
and glycolic, glyoxylic, and
oxalic acids in the case of
ethylene glycol.
SIGN AND SYMPTOMS OF TOXICITY

If untreated, methanol ingestion


may produce blindness,
metabolic acidosis, seizures, and
coma. Ethylene glycol
ingestion may lead to renal
failure, hypocalcaemia,
metabolic acidosis, and heart
failure.
TREATMENT OF ALCOHOL TOXICITY

Fomepizole inhibits this oxidative pathway by blocking alcohol


dehydrogenase. It prevents the formation of toxic metabolites and
allows the parent alcohols to be excreted by the kidney

cofactors are administered to encourage metabolism to


nontoxic metabolites (folate for methanol, thiamine and
pyridoxine for ethylene glycol)

Hemodialysis is often utilized to remove the


already-produced toxic acids
Isopropanol (rubbing alcohol, isopropyl
alcohol)
This secondary alcohol is metabolized to
acetone via alcohol dehydrogenase. Acetone
cannot be further oxidized to carboxylic acids,
and therefore, acidemia does not occur.
Isopropanol is a known CNS
depressant(approximately twice as
intoxicating as ethanol) and GI irritant.No
antidote is necessary to treat an isopropyl
alcohol ingestion
BARBITURATE POSIONING

Barbiturates have been used as hypnotic and sedative agents, for


the induction of anesthesia, and for the treatment of epilepsy and
status epilepticus. They have been largely replaced by newer drugs.
They often are divided into three major groups according to their
pharmacologic activity and clinical use

 ultra–short-acting(THIOPENTAL)
 short-acting(SECOBARBITAL)
 long-acting(PHENOBARBITAL)
MOA OF TOXICITY

All barbiturates cause generalized


depression of neuronal activity in
the brain. Interaction with a
barbiturate receptor leads to
enhanced gamma-aminobutyric
acid (GABA)–mediated chloride
currents and results in synaptic
inhibition. Hypotension that
occurs with large doses is caused
by depression of central
sympathetic tone as well as by
direct depression of cardiac
contractility.
SIGN AND SYMPTOMS OF BARBITURATE TOXICITY

The onset of symptoms depends on the drug and the route


of administration.
 Lethargy, slurred speech, nystagmus, and ataxia are
common with mild to moderate intoxication.
 With higher doses, hypotension, coma, and respiratory
arrest commonly occur.
 With deep coma, the pupils are usually small or mid-
position; the patient may lose all reflex activity and
appear to be dead.
 Hypothermia is common in patients with deep coma
TREATMENT OF TOXICITY

There is no specific ANTIDOTE for BARBITURATE POISONING


EMERGENCY & SUPPORTIVE MEASURES:
 Airway protection
 Treat COMA, HYPOTHERMIA and HYPOTENSION if they occur
 For COMA, focus on the following treatment principles DEXTROSE
 For ADULTS (50% solution, 50 ml. I.V)
 for CHILDREN (25% solution, 2 ml/kg I.V)
 THIAMINE : 100 mg (I.V)
 NALOXONE : Initially 0.4 mg I.V. If no response to therapy  give 2 mg
I.V  if no response to therapy  give 10-20 mg I.V
DIGITALIS POISONING

One of top toxins in the world because


of the wide availability of digoxin and a
narrow therapeutic window. Digitalis is
a plant-derived cardiac glycoside
commonly used in the treatment of
congestive heart failure (CHF),atrial
fibrillation, and reentrant
supraventricular tachycardia. Digoxin-
specific fragment antigen-binding
(Fab) antibody has contributed
significantly to the improved morbidity
and mortality of toxic patients
MOA OF DIGITALIS
TOXICITY

Most of digoxin effect in HF patients is


thought to be due to ANS modulation. But
Toxic effects are explained mainly by
excessive Na-K pump inhibition.

Toxic effects of digoxin


 Arrhythmias occur when the cytoplasmic
[Ca] increases to concentrations
exceeding the storage capacity of the
sarcoplasmic reticulum.
 As a consequence of this internal [Ca]
overload, several cycles of Ca release–
reuptake are required to restore the Ca
equilibrium between sarcoplasmic
reticulum and cytoplasm
SIGN AND SYMPTOMS OF DIGITALIS TOXICITY

NONCARDIAC TOXICITY Cardiac toxicity

 Anorexia  Ventricular arrythmias


 Vomiting  Atrioventricular block
 Abdominal pain  Atrial arrythmias
 Visual disturbance  Sinus bradycardia
 Halos
 Photophobia
 Fatigue
 Weakness
 Confusion
 Delirium
 psychosis
TREATMENT OF DIGITALIS
TOXICITY

 Stop digitalis administration


 DIGOXIN antibody(digibind fragment) is
used specially to treat life threatening
digoxin overdose, particular
hyperkalemia
 ANTIARRYTHMIC
 1:Lidocaine I.V for ventricular arrythmias
 2:Atropine I.V for bradyvardia or heart
block

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