Professional Documents
Culture Documents
Metals
Metals
Excreted in urine after short period of exposure and persist for days or months
trichloride
Most of theme are not affected by putrefaction (can be detected after long time
The morbidity rate is variable, but the mortality rate usually approximates 100%
Arsenicals have been used since ancient times as drugs and even today are very
Na, K arsenites
Copper arsenite
(Paris green)
trivalent.
Organic Salts ( Medicinal Forms of Arsenic)
They are used as general tonics treatment of some diseases e.g. black head
Absorption
From the GIT depending on the solubility and stomach content
Arsenites (trivalent) are more toxic (more soluble) than arsenates (pentavalent)
Arsenite methyl transferase (AS3MT) to improves metabolism and flushes out the
toxin faster.
Routs of Exposure
Using unclean utensils of arsenic dips, weed killer, insecticides, foot-rot bath and
dips
Contaminated herbage by arsenical preparations
Staggering gait
Collapse
Paralysis
Symptom of Acute Toxicity
Depending on :-
Subnormal temperature
Nervous manifestations
Incoordination & Paresis
Blindness
GIT- Manifestations
Thirst & Indigestion
Loss of appetite and body weight (poor growth)
Anemia
Blindness
GIT- Manifestations
Thirst & Indigestion
Skin disturbances
Necropsy Findings (PM)
Rose-red inflammation of GIT especially the stomach
After death is mainly performed in liver kidney hair hoof and tissues
gravity, and urinary casts have been reported as a result of renal damage.
Symptomatic treatment
Given every 4 hr for 2 days, every 6 hr on the 3rd day, and twice/ day for the next
10 days or until recovery
Pencillamin & Ca-EDTA
The mortality rate is high among animals acutely poisoned with inorganic
arsenicals.
Animals poisoned with pentavalent organic arsenicals can experience a high
morbidity rate, but with good nursing care a low mortality rate.
Recovery may require 2 to 4 weeks.
Antimony
Poisoning
Forms and Occurrence
Antimony is used with lead alloys, in batteries, rubber, ceramics, enamels and paints
Inorganic compounds
Antimony oxide was used in feeding geese in Europe to produce enlarged liver
(voagra)
Antimony trichloride (butter of antimony) used in dehorning, canker of hoof in horse
and foot-rot in sheep
Antimony trioxide is used as a fire retardation in plastics, textiles, rubber, and paper
Distribution
In all organs; mainly in liver and lung in case of inhalation
Metabolism
Pentavalent is reduced in the cells to the trivalent
Excretion
Mainly in feces, also in urine and through skin
Mode of Action
It inhibits phospho-fructokinase thus reduces the cell ability to utilize glucose
Chronic form
Aphthous patches on the buccal cavity
Toxic myocarditis
Fatty degeneration and necrosis of liver and kidney
Stimulants
Treatment
Keep the animal warm with high fluid intake
hydrargyrum
Forms and Occurrence
•Mercurochrome
•Fungicides
•Purgative powder •Hg chloride - Methyl Hg chloride
• Parasiticidal (Corresive sublimate) - Methyl Hg acetate
• Counter irritant •Mercurous chloride -Ethyl Hg
ointments (calomel) • Dimethyl Hg
• improper disposal •Red Hg iodide • Ethyl Hg
of fluorescent lamps •Hg cyanide •Diuretics
- Mersalyl
- Salyrgan
Mercury Toxicity
Hg2+ (mercuric II) are more toxic than Hg22+ (mercurous I) because its solubility in
water is greater (more absorbed from GIT)
Dimethyl mercury, is the most dangerous mercury compound (few microliters
spilled on the skin, or even a latex glove can cause death)
Mercury vapor emitted from amalgam tooth fillings
Methyl mercury in edible tissues of fish
Methylation of Mercury
Biomagnification: Methyl Hg is bio-concentrated it in the food chain of the human,
large carnivorous and fish. High species on the food chain accumulate mercury
ten times higher than the species they consume (Minamata disease)
Mechanism of action
A significant portion of mercury vapor crosses the blood–brain barrier and placenta before it
is oxidized by erythrocytes, and thus shows more neurotoxicity and developmental toxicity.
Liquid element & inorganic salts are slightly absorbed from GIT and skin
Organic salts (MeHg & di MeHg) from the GIT, lung and dermal even from intact skin
Dogs and cats are most susceptible to poisoning from mercurial ointments (absorption from
skin and licking of the applied part)
Distribution
All over the body
Excretion
Inorganic mercury: mainly in urine and some in feces, saliva, sweat and milk
Severe diarrhea
Anorexia
Colitis
Renal signs
Rare in inorganic toxicity, common in chronic (acute nephritis)
Oliguria may progress to anuria and ended with death
Nervous signs
Weakness, Stiff stilted or staggering gait, incoordination progress to paresis and
paralysis and mental disturbance
Pigs showed blindness, inability to eat and continuous walking
Alopecia, scabby lesions around anus and vulva skin rashes and dermatitis
Renal signs
Anuria due to
Tubular obstruction
Increased back diffusion of tubular filtrate
Preglomerular vasoconstriction
Na thiosulphate IV or orally
Treatment
Alkaline diuretics as K nitrate or Na gluconate 10%
In case of skin absorption, wash with soap and water
Contamination of water supply passing through lead pipes (water rich in nitrates)
or contaminated pasture and soil near lead works (Run off water via pipes before
drinking)
Wild Birds ingest the spent lead shots or bullets
10% is absorbed
Respiratory system
Storage
Acute toxicity in soft tissues, kidneys & liver
Excretion
Feces (Bile)
Common in calves, in farm animals, especially cattle and sheep with high mortality rate
uncommon in horses
Sudden onset of signs and a short course (12-24 h) or death without signs
Snapping of eye lids, rolling of eyes, pupil dilatation and blindness with circling movement
Cattle
Mania, charging into fences, climb walls, circling move and pressing the head
against fixed objects
Ruminal atony, constipation then offensive diarrhea.
Symptoms of Acute and Subacute Toxicity
Horses
Inspiratory dyspnea due to paralysis of the recurrent pharyngeal nerve
Aspiration pneumonia
Dogs
GI disturbance in old while nervous disturbance in the young
Poultry
Depression
Excessive thirst
Blue-black line or lead line on gum in horses, man and carnivores, due to the presence of
lead sulphide, not occur in cattle due to the failure to form tartar
Long bone Radiograph of knee “lead lines” with blood lead
level of 10.6 µg/dL. Notice the increased density on the
metaphysis growth plate of the knee, especially in the femur
PM Findings
Increased R/F ratio in blood (more than 3 indicate toxicity, less than 1 the species is
resistant as pig, rabbit, chickens)
Blood incubated with δ-ALA; the formed porphobilinogen is measured (E1) indicating
free (F) δ-ALAD.
Addition of glutathione to the sample reactivates the blocked part of the enzyme by
lead. Total enzyme activity is measured again (E2).
Reactivated (R) =E2 - E1
Treatment
Acute lead poisoning in cattle always fatal
General treatment
Remove lead from the GIT by:
Rumenotomy
Emetics
Precipitating antidotes
Na sulphate, Mg sulphate, milk, egg white and tannic acid (ppt Pb as insoluble sulphate,
albuminates or tannate)
Immobilization of lead in a harmless form in bone by Ca and vit D
Treatment
Increase lead elimination from the body by K citrate & Na thiosulphate (urinary
alkalinizers)
Specific treatment
Calcium versenate (Ca Na2EDTA)
Injection of D. pencillamine
A milkman has an 8-liter container full of
milk, and also two empty containers that
measure 5 liters and 3 liters. He needs to
deliver 4 liters of milk to a customer.
Reward
The milkman has no other spare containers
and no way to mark any containers. He
does not want to pour milk away. How will
he measure the 4 liters of milk?
The Answer
1. Fill the 5-liter container.
2. Pour out from the 5-liter container to the 3-liter one until it's full. The 5-liter
container now has 2 liters left.
3. Pour all the milk from the 3-liter container back to the 8-liter container.
4. Pour the 2 liters from the 5-liter container to the 3-liter container. It has therefore
just one liter of space left!
5. Fill the 5-liter container.
6. Pour out from the 5-liter container enough milk to fill the 3-liter container (which
already has 2 liters). You will have 4 liters left in the 5-liter container.
POISONING
Forms and Occurrence
Has long biological half life and cumulative effect
Used as:-
Distribution:
Bound to RBCs and serum albumen then to soft tissues in kidney & liver forming
Cd. metallothionine
Stored in association with metallothionein for long time in liver &kidney (Cd-
metallothionein complex has protective effect)
Toxicokinetic
Excretion
The unabsorbed Cd (95% ) in feces
Urine contains:-
High amounts of Cd & Calcium
General treatment
Prevent more exposure to Cd
Specific treatment
BAL alone is not preferable
The efficacy of EDTA is improved with concomitant use of glutathione (protects against
nephrotoxicity) and antioxidants as thiamine, zinc or methionine
D-pencillamine
Fungicides
Wood preservatives
Rodenticide
Toxicokinetic
Absorption
GIT
Respiration
Skin
Distribution
Absorbed F is transported to liver then to bone and teeth (90%), to placenta and soft
tissues
Storage
in teeth and bones
Excretion
Mainly in urine then faeces, milk and saliva
Mode of Action
GIT irritation
interfere with
Cardiovascular kidneys
Ca & P blood
Anti Nervous system
Hyperesthesia
Myocarditis
excretion coagulant Tetani
Mode of Action
Enzymes inhibition
AChE
Aconitaze enzyme
Bone Teeth
Teratogenic action
Protoplasmic poisonous
In advanced cases, skeletal fluorosis causes pain and damage to bones and
joints
Osteosclerosis elevation in bone density detected on a radiograph as an area of
increased opacity where more mineral is present
with/without osteoporosis (decrease in bone mass and density)
Skeletal fluorosis
Dental fluorosis
May occur in permanent teeth before
eruption
Mottling, pigmented spots or bands
(yellow to brown)
Excessive and irregular erosion
Painful teeth & loss of body weight
Eruption of abnormal teeth
Hypoplasia of enamel and dentine
Enlarged lower jaw
Gum damage
PM Findings
Chronic poisoning
Chalky Bones (white appearance and brittle)
Bone exostosis
Narrowing of BM cavity
Mottling of teeth
blood
Gastrointestinal sedatives
Vit. C