Download Acids and Alkalis

Acids and Alkalis
Caustic Agents
Acids and Alkalis
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Corrosives - denotes an acidic substance
Caustics - denotes an alkaline substance
Federal Hazardous Substance Act of 1967
Cause tissue injury by a chemical reaction - accept
(base) or donate (acid) a proton.
Severity of tissue injury is determined by:
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the substances pH or pKa,
concentration,
duration of contact and
volume of contact.
Acids and Alkalis
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Ingestion is an extremely common event, accounts
229,500
alkali drain cleaners and acidic toilet bowl cleaners
are responsible for most fatalities
10% of caustic ingestions result in severe injury
requiring treatment
between 1-2% result in stricture formation
80% of ingestions are in children > 5 years
most adult ingestions are intentional
Acids
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Mechanism of action - denature proteins
• coagulative necrosis
• cell morphology not grossly altered, destruction of
enzymatic proteins
• acid burns cause formation of tough leathery eschar
or coagulum (which sloughs in 3-4 days)
• little to no systemic absorption
• stomach is most commonly involved organ
Acids, cont.
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Management - any ingestion constitutes a
medical emergency
skin or eye contact • flush with copious amounts of water. remove
contact lens and jewelry
• wash skin with mild soap
• do not apply topical ointments, creams, or
dressings
Acids, cont.
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Ingestion
• serious solid ingestions are rare as the particles
usually stick to the oropharynx, but liquid exposures
can be severe
• burning is so severe patient probably can not
swallow
• do not give carbonated beverages
• do not give water, water + acid explosive release of
steam - exothermic reaction
• do not induce vomiting
• maintain airway
Acids, cont.
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Clinical concerns:
• perforation may occur after the third to
fourth day as eschar sloughs
• gastric outlet obstruction may develop over a
2-4 week period
• upper GIT hemorrhage
Acids, cont.
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Common acid containing sources
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toilet bowl cleaners
automotive batteries
rust removal porducts
metal cleaning products
drain cleaning products
Acids, cont.
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Boric acid - H3BO3
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weak bacteriostatic agent
used as an insecticide for roaches (roach motels)
do not apply to open wounds
toxic to the kidneys
can cause a severe dermatitis - boiled lobster rash seen on palmar and plantar surfaces and buttocks
Acids, cont.
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Carbolic acid - phenol
• one of the oldest disinfectants known
• used as a deodorizer - Lysol
• absorbed through intact skin
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Signs - nausea, diaphoresis, CNS
stimulation, hypotension, renal failure
Treatment - demulcents, activated charcoal
Alkalis
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More common cause of toxicity than acids
Most common alkaline agents causing toxicity
• Ammonia
• Sodium hydroxide
• both of these are found in household cleaners and
drain cleaners
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Most cases are in children under the age of
five years
Alkalis, cont.
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Mechanism of action
• tissue injury causes by liquefactive necrosis
(saponification of fats and solubilization of proteins)
• cell death occurs from emulsification and disruption
of cell membranes
• OH ion reacts with tissue collagen causing it to swell
and shorten
• most severe injured tissues are the squamous
epithelial cells of the oropharynx and esophagus (the
most commonly involved organ)
• alkali burns to the skin are yellow, soapy and soft
Acids, cont.
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Clinical concerns
• tissue edema - leading to possible airway
obstruction
• erythema
• ulceration
• necrosis of tissues with possible stricture
formation (depends on depth of burn)
• perforation can occur
Alkalis, cont.
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Management of toxicity
• eye and skin contamination - flush with copious
amounts of water
• ingestion - any ingestion constitutes a medical
emergency
• do not induce vomiting
• give demulcents (milk, water or egg whites)
Alkalis, cont.
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Common base containing sources
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drain cleaning products
ammonia - containing products
over cleaning products
swimming pool cleaning products
automatic dishwasher detergent
hair relaxers
clinitest tablets
bleaches
cement
Alkalis, cont.
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Disc batteries
• usually pass through GIT in 48 hours
• can become lodged
• pressure necrosis
• leak out potassium or sodium hydroxide
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Soaps - most are non toxic
• have emetic action so vomiting is spontaneous
• automatic dishwashing soap - highly corrosive
Alkalis, cont.
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Ammonia - NH3 - at room temp is a highly H2O
soluble, colorless, irritant gas with a pungent odor.
1993 anhydrous ammonia was the 3rd most produced
chemical in the US
farmers use 1/3 for fertilizer and animal feed
A component of may household cleaning products glass cleaners, toilet bowl cleaners, metal polishes, etc.)
highly alkaline and corrosive
• household ammonia - not as corrosive
Alkalis, cont.
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Most common mechanism is exposure to anhydrous
ammonia - liquid or gas
• NH3 + H2O ------ NH4OH
• this reaction is exothermic - causes significant thermal injury
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Ammonium hydroxide also causes severe alkaline burns
 1998, US PCC reported 6,000 cases, 95% accidental,
13% resulted in moderate to severe outcomes
 Ingestion of household solutions is usually accidental
and occurs in young children, adult ingestions are
usually suicide attempts
Alkalis, cont.
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Typical household ammonia
• contain 3-10% ammonia hydroxide
• pH less than 12.5 - caustic burns usually only seen
with pH’s >12.5 so household products do not
typically lead to significant burns
• patients present with oropharyngeal and epigastric
pain
• may cause aspiration pneumonitis
• kids may bite smelling salts - 20% ammonia - can
cause esophageal burns and mild respiratory
symptoms
Alkalies, cont.
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Bleach - sodium hypochlorite - NaOCl
• taste terrible and spontaneously vomited
• never mix bleach with acid or alkaline cleaning
agents - release of chlorine gas
• good to apply topically for any bites
Hydrocarbons
Hydrocarbons
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Organic compounds containing H and C
Derived from plants or from petroleum
distillates
3 basic types
• aliphatic
• aromatic
• halogenated
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Petroleum distillates - produced from
fractional distillation of crude petroleum
Terpenes - distillates of pinewood
Hydrocarbons, cont.
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Examples of petroleum distillates
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kerosene
gasoline
mineral spirits
naphtha
mineral seal oil
diesel oil
fuel oil
Hydrocarbons, cont.
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Characteristics
surface tension - cohesiveness of molecules
on the surface of a liquid
volatility - tendency of a liquid to change
into a gas or vapor
viscosity - resistance of a substance to flow
over a surface, directly relates to the
aspiration hazard
• low verses high viscosity
Hydrocarbons, cont.
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Mechanism of Toxicity
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64, 634 cases of HC exposure in 1994, as reported by
the American Association of Poison Control Centers
24% required hospital treatment
more than 1/2 of all exposures occur in children under
the age of 6 years
most exposures are accidental
22 people died in 1994
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Hydrocarbons, cont.
Mechanism of toxicity, cont.
 major threat is danger of aspiration pneumonitis
 vomiting increases the risk of aspiration
 when aspirated, petroleum distillates :
• inhibit surfactant - causing alveolar collapse and
resultant hypoxemia
• cause bronchospasm and capillary damage
• cause hemorrhagic bronchitis
• cause pulmonary edema
Hydrocarbons, cont.
Mechanism of toxicity, cont.
 Systemic toxicity can occur after oral
ingestion
• CNS depression, GIT irritation, liver and
kidney damage, cardiovascular toxicity
Hydrocarbons, cont.
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Characteristics of poisoning, 3 organ systems
usually involved:
Pulmonary, GI & CNS
Signs and symptoms of pulmonary involvement
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coughing, gasping and choking
smell of gasoline to the breath
rales and wheezing upon auscultation
hemoptysis and pulmonary edema
Hydrocarbons, cont.
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Signs and symptoms of GIT involvement
• irritation of oropharynx
• nausea and vomiting
• abdominal pain
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Signs and symptoms of CNS involvement
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cerebral hypoxemia
lethargy
somnolence
coma or seizures
Hydrocarbons, cont.
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Management of poisoning
To induce vomiting or not to induce
vomiting
Do not induce vomiting in patients who
have ingested low viscosity petroleum
distillate hydrocarbons ingestion as it
increases the risk of aspiration
pneumonitis
Do Maintain airway and support
respiration
Hydrocarbons, cont.
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Do induce vomiting in patients who have
ingested:
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halogenated hydrocarbons
insecticides
turpentine
aromatic hydrocarbons
or ones which contain of heavy metals - must
protect airway (endotracheal intubation)
Hydrocarbons, cont.
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Terpenes
include pine oil, turpentine, and camphor
 pine oil - product of pine trees (Pine Sol)
 turpentine is a distillate from pine trees
 camphor - distillate of the camphor tree
 Have lower volatility and higher viscosity
therefore less of a risk of aspiration than the
petroleum distillates
Hydrocarbons, cont.
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Mechanism of Action of Turpentine and Pine oil
Systemic toxicity results in GIT irritation and
CNS depression
• see nausea, vomiting, diarrhea, weakness,
somnolence, stupor and coma
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Treatment:
• GI tract decontamination - induce vomiting
• maintain airway
• transport
Hydrocarbons, cont.
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Camphor
• uses - OTC preparations such as local anesthetics,
chest cold inhalants, etc.
• basically no therapeutic value, but still used
• problem occurs if it is ingested
• can cause CNS excitation and seizures, mechanism
of action is unknown
• causes irritation of upper airway and mucous
membranes
• Treatment - supportive care
Toxic Gases
Carbon Monoxide
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The most common form of poisoning
From 1979 to 1988, 56,000 people died from CO
Colorless, odorless, nonirritating gas
Produced by incomplete combustion of carbon
containing compounds
Combines with Hb to form carboxyhemoglobin
CO-Hb will not transport O2
T 1/2 of CO-Hb is 5-6 hours in room air, 90 min in
pure O2 at 1 atm, 23 min in O2 at 3 atm
Carbon monoxide, cont.
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Sources:
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propane powered engines
natural gas appliances - space heaters
automobile exhaust
gas log fireplaces
kerosene heaters
hibachi grills
portable generators
Carbon monoxide, cont.
Mechanism of action:
 Competes with O2 for active sites on Hb (220x
the affinity for Hb as O2)
 Interference with cellular respiration at the
mitochondria level, binds to cytochrome oxidase
 Induces smooth muscle relaxation
 Hypoxemia, tissue hypoxia, no cyanosis, CO-Hb
is cherry red in color
Carbon monoxide, cont.
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Diagnosis based on patient presentation and a
good history
Signs and symptoms vary widely
Signs depend on % CO-Hb levels in the blood
Presence of cherry red blood is pathognomonic
Carbon monoxide, cont.
Clinical grading of CO poisoning
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Mild
• headache, nausea, dizziness, vomiting, flu like
symptoms
 Moderate
• confusion, slow thinking, shortness of breath, blurred
vision, tachycardia, tachypnea, ataxia, weakness
 Severe
• chest pain, palpitations, severe drowsiness,
disorientation, hypotension, syncope, myocardial
ischemia, pulmonary edema
Carbon monoxide, cont.
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Exposure during pregnancy can be teratogenic
Chronic low level exposure can cause:
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tiredness
lethargy
irritability
visual impairment
increased incidence of heart disease on
atherosclerosis
Carbon monoxide, cont.
Management of Toxicity:
 The antidote for CO poisoning is 100%
oxygen
 hyperbaric chambers should be used
more frequently than they currently are
in the treatment of CO poisoning
Hydrogen sulfide poisoning
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Highly toxic, malodorous, intensely irritating gas
 Sources:
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decaying organic materials
natural gas
volcanic gas
petroleum
sulfur deposits
sulfur springs
Most exposures are occupational
Hydrogen sulfide, cont.
Mechanism of action:
 inhibits mitochondrial cytochrome oxidase
 paralyzes the electron transport system
 inhibits cellular utilization of O2
 metabolic acidosis secondary to anaerobic
metabolism
 plenty of O2 in the bloodstream, cells can not
utilize it, so no hypoxemia but tissue hypoxia
Hydrogen sulfide, cont.
Mechanism of action, cont.:
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more potent cytochrome oxidase inhibitor than
cyanide
 rapidly absorbed through the inhalation route
 metabolized by the liver and excreted through the
kidneys
 cause of death is respiratory paralysis due to toxic
effects of H2S on respiratory centers in the brain
Hydrogen sulfide, cont.
Concentration (ppm)
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0.02
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100-150
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250-500
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500-1000
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>1000
Clinical effect
odor threshold
nose/eye irritation,
olfactory nerve paralysis
sore throat, cough,
keratoconjunctivits, chest
tightness, pulmonary edema
headache, disorientation,
loss of reasoning, coma,
convulsions
death
Hydrogen sulfide, cont.
Treatment:
 rescuer protection
 basic life support
 give O2, hyperbaric oxygenation is beneficial
 nitrates are antidotal by inducing Meth-Hb providing a large available source of ferric-heme
which has a greater affinity for H2S than does
cytochrome oxidase, sequestering sulfide ions
freeing cytochrome oxidase
Cyanide
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Hydrocyanic acid, Prussic acid
In 1994 only 360 cases of cyanide poisoning (300
were unintentional, 9 patients died)
Sources:
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electroplating, jewelry and metal cleaners
photographic processing
fumigant rodenticide
criminal tampering with OTC capsules
Amygdalin - pits of peaches, cherries, apricots,
apples, plums
• laetrile
Cyanide, cont.
Mechanism of action:
 causes tissue hypoxia by binding with ferric iron of
mitochondrial cytochrome oxidase, thus inhibiting the
functioning of the electron transport chain and the cells
ability to utilize O2 in oxidative phosphorylation
 substantial decrease in ATP production
 see a shift to anaerobic metabolism
 increased lactic acid production - metabolic acidosis
Cyanide, cont.
Clinical presentation:
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tissue hypoxia, especially of the heart and brain
(plenty of O2 in the bloodstream, cells can not
utilize what is there)
signs depend upon route and dose
inhalation of cyanide gas usually produces
rapid death
delayed onset after exposure to Amygdalin
Cyanide, cont.
Clinical presentations, cont.
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Patients who do not experience sudden collapse you will
see anxiety, hyperventilation, CNS stimulation,
tachycardia, palpitations
 Late signs of poisoning include nausea, vomiting,
hypotension, generalized seizures, coma, apnea, a variety
of cardiac dysrhythmias
 Smell of bitter almonds to the breath
 Absence of cyanosis
Cyanide, cont.
Treatment:
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amyl nitrate - to induce Meth-Hb (same
as with H2S)
give O2
Heavy Metal Toxicity
Mechanism of Action
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Most common route of exposure is oral
• secondary is inhalation of fumes
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Toxicity is expressed biologically because
of their ability to bind to one or more
ligands of biologic enzyme systems which
then inactivates the enzyme system
One of the few poisons that we
have a chemical antidote for:
Chelating Agents
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Chemical antidotes - chemically inactivate the
poison
Compete with enzyme systems for the metals
Reverse the metals toxic effects
Enhance the excretion of the metal
The chelate formed is a stable compound
Chelates are water soluble
Chelates are excreted by the kidneys
Chelating Agents, cont.
How effective these chelating agents are
depends upon:
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1) the affinity of the chelator for the metal
 2) distribution of the chelator to the parts of the
body where the metal is
 3) ability of the chelator to mobilize the metal
from the body once the chelate is formed
Chelating Agents, cont.
Properties of the ideal chelating agent:
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1) greater affinity for the metal than for ligands of
tissues
2) high water solubility
3) can penetrate into tissues
4) resistant to metabolic degradation by the body
5) forms a tight stable bond with the metal which
is non toxic to the body
Chelating Agents, cont.
Properties of the ideal chelating agent, cont.
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6) be readily excreted unchanged
 7) low affinity for calcium
 8) minimal inherent toxicity
 9) be absorbed readily when given orally
Chelating Agents, cont.
 No
drug has a single effect,
drugs are two edged swords.
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Examples of a chelating agent:
• calcium disodium EDTA - can cause renal
problems, fever, dermatitis, used to treat lead
toxicity
Heavy Metals
Lead toxicity
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Sources - used in the past in medicines
(sugar of lead), insecticides, pesticides,
gasoline (tetraethyl lead), batteries, paints,
manufacturing, automobile exhaust.
The fall of the Roman empire was due to
the fact they used lead for pipes to carry
water and for drinking goblets and utensils.
Lead Toxicity, cont.
Clinical features, plumbism:
Acute intoxication: not common
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colic
metallic taste to mouth
vomiting, diarrhea or constipation
increased thirst
hemolysis, hemoglobinuria
oliguria
paresis and paresthesias
Lead Toxicity, cont.
Chronic lead intoxication - much more common
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Burtonian line - dark gray bluish black line on the
gingival margin (H2S + Pb = PbS)
Basophilic stippling (clumping of RNA)
Anemia
Colic, diarrhea, vomiting
Skeletal muscle weakness
Increase uric acid in blood
Headache, confusion, insomnia
Lead palsy (wrist drop and foot drop)
Lead Toxicity, cont.
Patient management:
 Acute intoxication - induce vomiting,
give cathartics, give proteins to delay
absorption (milk, egg whites),
chelating agents
 Chronic toxicity - give chelating agents
Iron Toxicity
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Seen mostly in children, 40, 000 exposures/yr.
Toxic doses:
• 20-60 mg/kg of elemental iron is potentially toxic
• 60-120 mg/kg is toxic but not usually fatal
• > 120 mg/kg is potentially fatal
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Only 10% of ingested iron is absorbed
Most iron tablets contain 10-30% elemental
iron by weight
Iron Toxicity, cont.
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Sources - dietary supplements
Clinical features:
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toxicity develops when serum iron levels exceed the
iron binding capacity of transferrin in the blood
 body is poorly equipped to handle excessive amounts of
iron - can eliminate only very small amounts/day
 free iron damages tissues by direct corrosive effects,
free iron is a potent vasodilators, directly injures blood
vessels, causes hepatocellualr death, coagulation
disturbances, and metabolic acidosis
Iron Toxicity, cont.
Clinical presentation of acute toxicity- 4 Stages
 Stage I - 30 min. to 6 hrs. post ingestion
Acute GI corrosive effects of iron, nausea,
abdominal pain, vomiting, and diarrhea,
hematemesis, hematochezia and melena.
Most patients with mild to moderate toxicity do not
progress beyond this phase.
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Stage II - 6-24 hours post ingestion
sometimes called the latent or quiescent period
transient resolution of patient’s GI signs
Iron Toxicity, cont.
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Stage III - 12-48 hours post ingestion
recurrence of GI hemorrhage, hematemesis,
melena and bowel perforation may be seen
acute circulatory shock, metabolic acidosis,
respiratory distress syndrome
death is common is this stage
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Stage IV - 4-6 weeks post ingestion
gastric outlet obstruction or pyloric stenosis as
a result of gastric scarring, vomiting
Iron Toxicity, cont.
Chronic toxicity:
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pigmented hepatic cirrhosis, diabetes mellitus,
hyperpigmentation of the skin, hemosiderosis
 hemochromatosis
Treatment:
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induce vomiting
 activated charcoal is of no value
 transport
 chelators
Mercury Toxicity
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Sources:
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Hg (Gr. - hydrargyros - water silver)
drugs (antisyphilitic agents, diuretics, cathartics,
topical salves), batteries, paint, shell fish, neon
lamps, thermometers, industry (“mad as a
hatter”), BP cuffs, wood preservatives, vaccines
dental amalgam fillings (50% mercury, 35%
silver, 13% tin, 2% copper with a trace of zinc)
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Mercury Toxicity, cont.
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Exists in nature in 3 major forms:
• organic (methyl mercury)
• inorganic
• elemental
Mechanism of Action:
• Forms covalent bonds with sulfide groups
disrupting many important cellular functions
Mercury Toxicity, cont.
Elemental mercury - quicksilver
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liquid at room temperature
vaporizes easily at room temperature
lung is major target organ due to inhalation of
volatilized fumes
lipid soluble and passes rapidly into blood
stream
see acute pulmonary symptoms, fever, chills,
dyspnea, lethargy, confusion, vomiting
Mercury Toxicity, cont.
Elemental mercury - quicksilver, cont.
 Chronic exposure - tremors, gingivitis,
insomnia, shyness, memory loss,
anorexia, depression
 ingestion is usually no problem - poor
absorption from GIT
Mercury Toxicity, cont.
Inorganic mercury - mercurial salts
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route of exposure - oral
source - disc batteries, mercurous chloride,
vaccines (0.01% thimerosal)
clinical signs associated with the caustic effects
signs and symptoms - pain, vomiting,
hematemesis, renal failure
Mercury Toxicity, cont.
Organic mercury:
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source - contaminated food products, methyl
mercury contaminated seafood in the 1950’s in
Japan killed over 1000 people (Minamata Bay)
elevated levels found in blood stream of mothers
and infants - source? (tuna)
major signs and symptoms are neurological,
visual field constriction, ataxia, paresthesia,
hearing loss, muscle tremors, and even death
Mercury Toxicity, cont.
Diagnosis is based on:
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patient history and clinical signs
urinary levels of mercury (values greater
than 20-25 ug/L is abnormal)
Treatment:
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acute therapy - same as any poison
chronic - chelation therapy (BAL)
Arsenic Toxicity
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Commonly found throughout the earth’s
crust, contaminates well water
used in manufacture of herbicides and
pesticides and computer chips
tasteless and resembles sugar
has been used as a therapeutic agent and as
a poison for more than 2000 years
most exposures are accidental and deaths
are very rare
Arsenic Toxicity, cont.
Mechanism of action:
 Inhibition of sulfhydryl group-containing
cellular enzymes and the replacement of
phosphate molecules in “high energy”
compounds
 Trivalent arsenic is a carcinogen (lung and skin
cancer) and is the most toxic form
 Toxic dose ranges from 1 mg to 10 grams
 Can be recovered from the hair, nails and skin
Arsenic Toxicity, cont.
Clinical presentation:
 Acute exposure
• burning of the mouth and throat, nausea,
vomiting, profuse diarrhea (rice water
stool), garlic like odor to breath,
increased capillary permeability, shock,
renal damage
Arsenic Toxicity, cont.
Chronic toxicity:
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skin pigmentation changes, palmar and plantar
hyperkeratosis
anorexia, GI symptoms
anemia (see pale patient with areas of increased
pigmentation and hyperemia - “Milk and Roses”
complexion)
Mee’s lines (white transverse bands in the nails)
metallic taste to the mouth
gangrene of the feet (“blackfoot disease”)
encephalopathy
Arsenic Toxicity, cont.
Diagnosis:
 Urine sample provide the most reliable
diagnostic testing, >200ug/L are abnormal
• use of hair or nails is generally not useful in
evaluating individual patients
Treatment:
 supportive care and chelation therapy
Natural Chelators
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Chlorella (from algae) is a natural immune
stimulant and has a high affinity for heavy
metals (it contains sulfur bound amino acids
and acts as a natural chelator)
Garlic and cilantro (Chinese parsley) aid in
the removal of heavy metals