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FLUOROACETATE

TOXIC

NAME

NO MATRIC

NURUL SHAHERA BT NIZAM

D20141066880

SITI SYAFIQAH BINTI ARIZAN

D20141066874

CASE 1 : FLUOROACETATE TOXIC


A man was found having nausea, vomiting and
abdominal pain, sweating, confusion and agitation
follow. His next of kin told the triage that he
accidentally swallow a rodent poison, which he
thought it is some kind of candy placed on the
kitchen table. The lab results were positive for
fluoroacetate toxic.
As a pathology researcher, you have to explain
the whole situation (biochemically) to a bunch of
industrial trainees in your pathology lab.

How the reaction occur ??


Fluoroacetate combines with coenzyme A (CoA-SH) to form
fluoroacetyl CoA, which can substitute for acetyl CoA in the
tricarboxylic acid cycle
Then, reacts with citrate synthase to produce fluorocitrate, (a
metabolite of which then binds very tightly to aconitase, thereby
halting the cycle).
Many of the features of fluoroacetate poisoning are, therefore,
largely direct and indirect consequences of impaired oxidative
metabolism.
Energy production is reduced and intermediates of the
tricarboxylic acid cycle subsequent to citrate are depleted

1. Acetyl CoA + OAA Citrate

[Hydration : Citrate

synthase]
2. Citrate Isocitrate

[Dehydration : Aconitase]

1. Fluroacetate + CoASH Fluoroacetyl CoA


2. Fluoroacetyl CoA fluorocitrate [use Citrate synthase]
3. fluorocitrate Isocitrate
Aconitase]

[inhibit by binding to

WHAT ARE THE IMPACTS?

Treatment for sodium fluoroacetate poisoning


is mainly symptomatic.
If ingested, vomiting should be induced immediately
followed by gastric lavage with two to four litres of tap
water and instillation of 15-30 g of saline cathartic.
Monoacetin (glyceryl monoacetate) 0.5 mg/kg should
be injected IM every half hour for 12 hours varying the
injection sites.

THE EFFECT OF PH ON THE


TOXICITY OF FLUOROACETIC ACID
The inhibition of oxygen consumption which is complete at much
lower concentrations of HFA likewise dependent upon the amount
of undis-sociated HFA in the cells environment.
The Inhibition Of Oxygen Consumption Is pH-Labile,Which
Indicates Either That The Inhibitory Agent Is Dissociable,Or
That The Metabolic Reactions Of The Cell Change With Variation
In Environmental pH.

Artificial respiration with the assistance of oxygen


may be required.
Calcium gluconate, 2-3 g per day in 10% solution
may be given IV.
To control convulsions barbiturates (preferably
phenobarbitone or pentobarbitone) should be given IM
or IV in sufficient dosage

T H AT S AL L
THANK YOU

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