ACUTE POISONING AND ITS

ANTIDOTE
WIDHARTO PH

INTRODUCTION

POISON:
SUBTANCE IN RELATIVELY SMALL QUANTITIES
CAPABLE TO PRODUCE DELETERIOUS RESPONS IN BIOLOGICAL
SYSTEM OR TO DESTROYING OF LIFE
POISONING:
EXPOSURE OF POISON IN THE BODY PRODUCING DAMAGE
RESPONSE TO HEALTH.
RELATED TO: - THE DOSE DELEVERD, FORM OF SUBSTANCE, TIME
AND FREQUENCY OF EXPOSURE, THE ROUTE OF EXPOSURE
THE MOST IMPORTANT TREATMENT ASPECT:
-SUPPORTIVE THERAPY TO MAINTAIN THE VITAL SIGN
-PREVENTING FURTHER ABSORPTION
- SPECIFIC ANTIDOTES
- ENHANCING OF EXCRETION

 CONTRA INDICATION USING EMETIC SUBSTANCE:

- COMATOSE, STUPOR, DELIRIUM
-CORROSIVE TOXIC SUBSTANCE
-CNS STIMULANT TOXIC SUBSTANCE
-PETROLEUM TOXIC SUBSTANCE
ANTIDOTES:
-PHYSICAL : ACTIVE CHARCOAL, MILK FLOUR, WHITE
OF EGG
-CHEMICAL: KMnO4 FOR ALKALOIDS, BAL FOR HAEVY
METAL
-PHYSIOLOGICAL: ATROPINE FOR PILOCARPINE

CYANIDES POISONING
Cyanide forms naturally in leucocytes and
neural cells, and also as a result of vitamin
B12 metabolism, and is also encountered
as a xenobiotic in plants containing
cyanogenic glycosides, such as cassava,
and tobacco smoke
Thiosulfate sulfurtransferase is a
mitochondrial enzyme encoded by the TST
gene that converts cyanide to the far less
toxic metabolite, thiocyanate.

The reaction involves transfer of sulfur from thiosulfate (or another

sulfur donor) as follows:
CN
+ S2O3 - SCN + SO3
Cyanide
thiosulfate
thiocyanate sulfite
Thiosulfate Sulfurtransferase (Rhodanese)
is a mitochondrial enzyme encoded by the TST gene that converts
cyanide to the far less toxic metabolite, thiocyanate

First, nitrites are administered in cyanide poisoning to form

methemoglobin, which then binds free cyanide, sparing
other critical cellular respiratory enzymes (Cummings,
2004).
Second, formation of cyanmethemoglobin by reaction of
hemoglobin with potassium ferricyanide is a standard
method for measurement of hemoglobin concentration.

Pesticides

Pesticides include all xenobiotics whose specific purpose is

to kill another form of life, including insects (insecticides),
small rodents (rodenticides), or even vegetation
(herbicides).
4(four) classes of pesticides :
1. organophosphates,
2. organochlorines,
3. organotins, and
4. carbamates.
Exposure to pesticides occurs most often in occupational
settings, in which manufacturers, those applying the
pesticides, or those harvesting treated agricultural
products, are exposed.

Organophosphates
Organophosphates include:
1.
malathion,
2.
parathion,
3.
methyl parathion, and
4.
diazinon
. neurotoxic effects of organophosphates are well
understood to occur via the inhibition of
acetylcholinesterase, the mechanism by which these
compounds suppress the immune system is not as welldefined.
. it is still unclear how the lymphocytic cholinergic
system (Tarkowski et al., 2004) contributes to
immunotoxicity

 Malathion exhibits both immune

suppressive and immune enhancing effects
Parathion has attracted more attention
than malathion, probably because it is
more acutely toxic
diazinon produced gross changes in the
spleen and thymus in response to acute
doses in mice (Handy et al., 2002;
Neishabouri et al., 2004). Diazinon also
suppressed humoral immunity

Organochlorines
The organochlorines include chemicals such as:
chlordane,
dichlorodiphenyltrichloroethane (DDT),
mirex,
pentachlorophenol,
aldrin, dieldrin, and
hexachlorobenzene
The organochlorines are among the longer-lived pesticides and they have an
increased propensity for contamination of soil and groundwater, thus providing
an additional route of exposure to the general population.
Many organochlorine compounds also act as xenoestrogens although it is unclear
as to whether the estrogenic effects of these compounds contribute to
immunotoxicity
Many organochlorine pesticides have also been associated with increased cancer
incidence (reviewed in Dich et al., 1997). The mechanism by which this occurs
is unclear but is likely multifaceted, including, in part, organochlorine-induced
modulation of the immune system