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Mechanism of Poisoning Clinical Manifestations (Signs & Symptoms) Management Therapy (Include Specific Antidote and MOA of Antidote)
Mechanism of Poisoning Clinical Manifestations (Signs & Symptoms) Management Therapy (Include Specific Antidote and MOA of Antidote)
Activity # 10
Metallic Poisoning
At the end of the practical class the student shall be able to:
Lesson plan:
Management
Therapy
Clinical
Mechanism (Include
Manifestations
Metal Sources of specific
(Signs &
Poisoning antidote and
Symptoms)
MOA of
antidote)
Mercury Volcanoes Mercury ions Acute exposure: Selenium, It is
Forestfire produce Initial signs and found in the
scannabar toxic effects symptoms, such enzyme
(ore) by protein as fever, chills, glutathione
fossil fuels precipitation, shortness of peroxidase.
such as coal enzyme breath, metallic This enzyme
and inhibition, taste, and protects the
petroleum. and pleuritic chest organism
generalized pain, may be against certain
corrosive confused with types of
action. metal fume damage. Some
Mercury not fever. Other data suggest
only binds to possible that Se plays a
sulfhydryl symptoms could role in the
groups but include body's
also to stomatitis, metabolism of
phosphoryl, lethargy, mercury (Hg).
carboxyl, confusion, and Selenium has in
amide, and vomiting. some studies
amine Chronic toxicity: been found to
groups. Chronic and reduce the
Proteins high-dose acute toxicity of Hg
(including mercury salts.
enzymes) exposure
with such produces a
groups variety of renal,
readily neurological,
available are psychological,
susceptible and cutaneous
to reaction symptoms. The
with exposed
mercury. individual may
Once bound experience
to mercury, rather vague
most and non-specific
proteins are symptoms,
rendered including
inactive. anorexia, weight
Toxicity is in loss, fatigue,
part related and muscular
to the weakness that
oxidative could be
state and to indicative of a
the chemical number of
form diseases.
(organic
versus
inorganic).
Silver Dust storms Main The lips are first The chemical
Fores fires mechanisms white from the antidote is
Volcanoes of toxicity is caustic action of common salt.
Diesel and that it the drug, then Soap and
engines causes become black. alkalies are
Cosmetics oxidative The vomited supposed to
Cigarette stress matter and the annul the
smoke through the discharges from poisonous
Lead and generation the bowels turn tendencies or
copper of reactive black upon to prevent the
Coal and coal oxygen exposure to the action of the
ash species and air. Convulsions, poison upon
Organic dust causes coma, paralysis, the mucous
damage to death may membrane of
cellular follow. the alimentary
components canal.
including
DNA
damage,
activation of
antioxidant
enzymes,
depletion of
antioxidant
molecules
(e.g.,
glutathione),
binding and
disabling of
proteins,
and damage
to the cell
membrane.
Gold Gold is primarily Gold binding Overexposure to
Dimercaprol, a
found as the pure, to thiol gold (as in
major protein
native metal. groups on treatment of
that is modified
Sylvanite and the hexose rheumatoid
by heavy metal
calaverite are gold- transport arthritis) may
toxicity is lipoic
bearing minerals. protein in cause skin
acid, which is
Gold is usually the rashes; bone
necessary for
found embedded in membranes marrow
pyruvate
quartz veins, or of blood depression;
dehydrogenase
placer stream cells can stomach and
and alpha-
gravel. alter glucose intestinal
ketoglutarate
metabolism bleeding;
dehydrogenase,
and thus headaches;
leading to the
may affect vomiting; focal
disruption of
the activity or generalized
the citric acid
and viability continuous fine
cycle and the
of cells. vibrating muscle
accumulation of
movements
pyruvic acid.
(myokymia);
and yellowing of Dimercaprol is
the skin, a dithiol that
mucous acts by forming
membranes, and
a stable five-
whites of the
membered ring
eyes (jaundice).
between its
sulfhydryl
groups and
certain heavy
metals, thereby
neutralizing its
toxicity and
promoting its
elimination.
Dimercaprol is
more
efficacious
when given
soon after the
metal exposure
because it is
better at
preventing
enzyme
inhibition rather
than
reactivating
enzyme
function.
Cadmium
Zinc
Aluminum
Manganese
Chromium
Nickel
Copper
Phosphorous
Stibium
Bismuth
Tungsten
Beryllium
Selenium
Arsenic
References:
https://watermark.silverchair.com/
https://www.sciencedirect.com/science/article/pii/S1021949814000118