Transcript Carbon Monoxide poisoning

Supportive or Symptomatic Treatment
11/4/2011
Management of Poisons in Conscious Patient:
1) Establish and stabilize adequate vital signs of Patient (CV, Respiration, CNS)
2) Clinical evaluation (Lab test, blood chemistry, liver enzymes)
3) Determine the cause for the symptoms (body temperature, pupil size, breath)
4) Removal of unabsorbed or the remaining portion of poison from the site of
exposure
* immediate action
*gastric emptying, (emesis, lavage,cathartics, neutralization,antidotes),
* enhance elimination (diuresis, changing urine pH),
* artificial & mechanical removal of the remaining poison)
5) Supportive & Symptomatic Treatment
6) Patient Disposition
7) Poison prevention
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Supportive or Symptomatic Treatment
5) Supportive & Symptomatic Treatment
a) General treatment strategy of relieving symptoms without actually
treating the cause (at this point, symptoms is treated and not the poison)
b) Regular medical treatment of each symptom separately (nausea &
vomiting, bleeding, changes in body temperature, CV, seizure, convulsion)
c) If the patient is suffers from acidosis, most likely is hyperkalemic ( K) &
has an electrolytes imbalance (Na+ & K), Na+ level needs to be adjusted
d) Adjust respiratory gases
e) If bradycardia develops, an external pacemaker may be necessary
f) If sever hypotension develops, an Intra-Aortic Balloon Pumps (IABP) is
inserted into the aorta to help maintaining blood pressure
g) If hyperthermia develops (ASA & salicylates can produce hyperthermia
& may lead to seizers in children), use of Tepid sponging (warm water) to
return the child normal temperature (also used for restless, tense patient)
h) Ice packs and alcohol sponging should not be used for toxic poisoning
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Disposition
• After released from hospital, patient should follow up with recommended
treatment for the specific symptoms
• Legal issues should be address:
– If toxicity is resulted from suicide or homicide attempted, authorities must be
notified
– Psychiatric should follow up regularly for the suicide cases
– If a child was overdosed, the case should be reported to Social Service
– Substances resulted in chronic effects, should be monitored & need follow up:
• acetaminophen (APAP) may cause delayed liver damage (liver enzymes must be
monitored regularly
• Iron overdose, may cause delayed mucosal effects & clotting deficiencies
• Any slow in improvement of the condition, patient should be referred to specialist
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Poisoning Prevention (1)
• Storage: medicines & chemicals should be stored safely out of reach &
out of sight of children, up high (at least 5-6 ft high) in a locked
or child resistant cupboard. Many poisonings occur when a product
or medicine is not in its usual storage location, when it is in use and
left on a bench top or bedside table, or during transport from shop to
home.
• Safe use: Use medicines and chemicals safely. Read directions for use
carefully. Do not leave them unattended whilst in use. Separate
medicines from household products.
• Identification: Be sure that all products are properly labeled. Read the
label carefully before use.
• Regular clean up: Clean out your medicine cupboard every several weeks.
Take unwanted and out-of-date medicines to your nearest
pharmacy for disposal.
• Children tend to imitate adults, so avoid taking medicines in their
presence.
• Refer to medicines by their proper names. They are not lollies.
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Poisoning Prevention (2)
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Watch the children at home: Visitors' bags may contain medicines. Keep them
well out of reach of children. Also, the incidence of poisoning increases when
usual household routines are disrupted (moving being on holiday, parties
and having visitors).
Use child resistant packaging: always ask for and use household and medicines
which are in child resistant packaging (e.g., blister or strip packs or special
push and turn lids).
Know what you are taken: Always take medicines in a well lit room, wear your
glasses. Follow the directions for use carefully and accurately. Do not take
other peoples medicines.
Use of house cleaning: Use appropriate protection when painting, spraying or oven
cleaning. Follow the directions for use. Protect skin and eyes. Ensure there is
adequate ventilation, with air circulating continuously. Remove any
contaminated clothing immediately.
Rinsing: all empty containers from liquid medications or household products
should be rinsed with water before they are thrown out.
Keep everything in original containers and never in cups or soft drink bottles.
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Agents-induced toxicity
• Hypoxia Producing Poisons
– Carbon monoxide
– Cyanide toxicity
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Corrosives and house hold cleaners toxicity
Toxicity of drug of abuse
Toxicity of therapeutic agents and drug overdose
Radiation toxicity
Pesticides/Insecticides and Insect Repellants toxicity
Rodentcidies and Herbicides toxicity
Heavy metals toxicity
Food Poisoning
Natural and other environmental toxins (i.e, Radon)
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Agents-induced toxicity
Hypoxia Producing Poisons
Carbon monoxide (CO) poison
• Endogenous & Environmental sources of CO:
• Produced endogenously in human body @ rate of 0.4 %/hr (breakdown of the
heme protein)
• The level is much higher in smokers (5-10% Carboxyhemoglobin COHb)
• CO produced as a result of incomplete combustion
• Burning Natural gas water heater, oil, coal, gasoline (garden tools), wood
burning stove/fireplace
• Faulty gas stoves, faulty space heaters, unclean chimneys, and car exhaust
– This has been used for the purpose of suicide (car exhaust)
Why CO is so treacherous: It is odorless, colorless, and
tasteless know as the silent killer
*** CO poisoning cause the death of 500 persons/year &
15,000 visit to the hospital emergency room/year (CDC)
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Hypoxia Producing Poisons
Carbon monoxide (CO) poison
* It has a high affinity for hemoglobin (250 times that of O2)
* It will also displace O2 very rapidly & decreases O2 dissociation from
hemoglobin (make O2 not readily available to the tissues, causing hypoxia
§ * Hypoxic hypoxia (Hypoxia to tissues as a result of hypoxia in the
blood)
§ * The brain and the heart are most affected
-The brain can not perform any anaerobic reactions (depends
on O2)
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Hypoxia Producing Poisons
Carbon monoxide (CO) poison
Symptoms of CO poisoning:
* < 10% (%= the amount hemoglobin converted to carboxyhemoglobin, COHg), no
serious symptoms
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* 20% - headache, tightness across forehead, dilation of blood vessels
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* 20-30%, visual disturbances, sever headache (brain function is affected),Tachycardia,
Tachypnea, Possible nausea and vomiting
* 30-40%, increased Tachycardia and Tachypnea, Syncope (fainting), inability to
leave the place where the poisoning is taking place
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* 50%, while in syncope, there is an increase in neuronal activity and convulsions
result, coma develops due to exhaustion of the CNS
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* 60% and higher, DEATH
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Carbon Monoxide Poisoning
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Carbon Monoxide Poisoning
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Carbon Monoxide Poisoning
* Populations with increased sensitivity to
CO (at high risk):
• o Anemic
• o Females, due to having less hemoglobin
• o Children, due to their high metabolic rate
• o Chronic Obstructive Pulmonary Disease
(COPD)
• o Hyperthyroid sufferers due to 
metabolic
rate
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Carbon Monoxide Poisoning
• * Treatment and Prevention of CO poisoning:
- Resuscitate the patient (ASAP, Sustain respiration, CNS, and circulation )
– - Give pure 100% O2
– - CO has a half-life of 4 hours (Carboxyhemoglobin). If we use 100% O2, we
will decrease CO half life to 40 minutes (Decreased chance for brain damage).
– - It the patient is placed into a hyperbaric chamber the CO half life will be
decreased even more to 20 minutes.
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Carbon Monoxide Poisoning
* * Treatment and Prevention of CO poisoning
* To get rid of the cerebral edema
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- Use an osmotic diuretic (Mannitol)
- Give a glucocorticoid (Prednisone) to decrease inflammation
- Due to anaerobic metabolism, acidosis may develop
• -Can lead to coma (give IV Na HCO3)
• -Can also cool the patient to decrease the demand of the CNS
• In any case, if one even suspect CO poisoning, do not hesitate to
call the National Poisoning Control Center 24/7. Do not wait
until is a matter of life and death
• Prevention: Install CO detector (every home should have one)
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Carbon Monoxide Poisoning
• * Outcome of CO poisoning
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§ Impairment of the CNS
§ Muscle Weakness
§ Depression
§ Parkinson’s –like symptoms
§ Decreased & blurred vision
§ Numbness in the extremities
§ Speech impairment
§ Paralysis
§ various degrees of symptoms may last for up to two years after the
incident
– § If exposure was the result of car exhaust fumes, then treat the CO
poisoning and also for alcohol intoxication.
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Hypoxia Producing Poisons
2) Cyanide Poisoning
• Cyanide is 1st isolated in pure form in 1786 by
Scheele from the dye Prussian blue
• Its sever toxicity was also discovered by Scheele
(was killed when inhaling the vapor)
• One of the most rapidly acting lethal poisons
known to the public
– i.e., homicidal disasters as the Jonestown massacre
33 years ago
– Cyanide-laced Tylenol in Chicago in 1982
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Cyanide Poisoning
• Cyanide (CN- ) negatively charged ion
• It present either in the gas form as Hydrogen
Cyanide (HCN), as a liquid or solid forms as
Cyanide salts
• At physiological pH 7.4 (unbound), in present in the
form of HCN
• HCN Can be formed when acid added to a Cyanide
salt
• It is concentrated in the RBC than in plasma (100:1)
• In RBC, 92-95% CN- is bound to Hb
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Cyanide Poisoning
Sources of exposure
1) Industry:
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electroplating (HCN gas or particulates in the air)
Extraction of Ores (gold and silver)
Metal processing
Manufacturing of plastics, pesticide, rodentcidies
Hair removal from hides (in tanning industry)
In pressure-treated wood (lumber)
Acetonitrile: a chemical widely used in
laboratories & some cosmetic removal is
metabolized to CN when ingested
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Cyanide Poisoning
Sources of exposure
2) Plants: (food/dietary supplements)
– Many plants (fruit pits of Apricot, Bitter Almond, Peach,
Plum) containing Amygdalin a cyanogenic glycoside, a
cyanide producing substance (glucose, benzaldehyde +
CN)
– The enzyme -glucosidase (found in these plants and in
human GI tract) will hydrolyze the glycosides  HCN
– Amygdalin (active ingredient in Laetrile) is hydrolyzed by
the enzyme emulsin (in GI)  HCN
– CN poisoning will develop if the kemels (i.e. Almond) is
eaten raw
– Once the kemels are processed, destroying the emulsin
and CN poisoning will not occur
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Cyanide Poisoning
Sources of exposure
3: Combustion:
- Small amount is endogenously produced in human
body
(Vit B12 metabolism)
- Polyurethane, a commonly used in modern plastic
furniture, release CN on combustion
– Silk and wool will release CN during fires
– Smoke inhalation, death will be due to both CO & CN
– Cigarette smoking (each release 150-200 g of HCN)
– Burning pressure treated wood in close place will
release HCN gas
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Cyanide Poisoning
Mechanism of Action
• Toxicity occurs by either respiratory, PO and dermal
routes.
• Produces cytotoxic hypoxia (interferes with cell
metabolism in the presence of normal blood and O2
supply) = metabolic inhibitor.
• HCN binds to heme iron in the cytochrome oxidase (aa3) (has high affinity for Fe+++) forming a complex
• This complex inhibits the final step of oxidative
phosphorylation where O2 is used for the production of
ATP
• Aerobic metabolism stops (cells will not be able to use
Q2), Patient essentially suffocates
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Cyanide Poisoning
Mechanism of Action
• Cyanide inhibits
mitochondrial cytochrome
oxidase , thus blocks
electron transport, resulting
in decreased oxidative
metabolism and oxygen
utilization
• Lactic acidosis occurs as a
consequence of anaerobic
metabolism (accumulation of
Lactic acid).
• Most affected cells are at the
heart & CNS
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Cyanide Poisoning
Symptoms
• Acute:
– Depends on the dose, route of exposure &
duration
• CNS (most sensitive), headache, nausea,
vomiting, confusion, restlessness & anxiety,
tachypnea with convulsion (are immediate, within
few min)
• Severe poisonings progress to tachycardia and
tachypnea, comma, fixed dilated pupils and death
(occur within minutes)
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Cyanide Poisoning
Symptoms
• Acute
• Skin/Ocular:
– In sever poisoning, skin is cold
– Cyanosis may be develop late
– Retinal veins and arteries may appears similar in color
• CVS: (required higher dose than that of CNS dose)
– Tachycardia followed by bradycardia
– Hypotension followed by peripheral vascular collapse
– Abnormal ECG & pulmonary edema
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Cyanide Poisoning
Symptoms
• Chronic:
– Long-term CN exposure  Occupational –related,
heavy smoker will cause headache, dizziness,
nausea, or vomiting, psychosis
– Tobacco Amblyopia: visual impairment not due to
lesion & abnormalities in the optic disk, but due to
direct effect of CN on the eye
• (Vit B12a) improve visual acuity in some patients)
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Cyanide Poisoning
Management
For prevention: small doses of Na+ Nitrite: (Sequesters CN before it gets
into the cells)
• * Give a mild nitrite by inhalation (2 pearls of Amyl Nitrite (crushed and
rubbed on the face)
• * Several drugs are used:
– 1) Amyl nitrite (by inhalation), followed by
– 2) Na nitrite (by IV), initial dose 300 mg/adult
– * these combination will convert Hb to methemoglobin and the
formation of Fe+++ heme
– * The Fe+++ will bind to CN forming a stable complex
Cyanmethemoglobin
– * As a result the free CN in circulation will ↓
• Be careful with the Nitrites, massive vasodilation and
server hypotension are possible
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Cyanide Poisoning
Management
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– * Permanent & irreversible intoxication of CN is by IV
injection of Na thiosulfate
– -25% Na + Thiosulfate 50ml, IV (Provides Sulfur for the
• enzymes Rhodanase)
- The enzyme Rhodanase converts CN to Thiocyanate
(inactive)
which is excreted in the urine
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Cyanide Poisoning
Laetrile
• * Used to be found in health food stores as a nutritional
supplement for malignancy
– *Obtained from the kemels of peaches, apricots, and almonds
• * Contain amygdalin (a cyanogenetic glycoside), CN is
liberated by the enzyme, emulsin (which works better
in
alkaline pH)
– - Used in more than 22 countries for cancer treatment
(falsely)
– - It kills cancerous and normal cells
- Children have a higher incidence of toxicity because
they have a more alkaline environment in their GI
- 2-3 tablets are lethal
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Toxicity induced by household
chemicals
1. Corrosive Alkalis
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Toxicity induced by household chemicals
1. Corrosive Alkalis
 *Occurs most often in Toddler’s and children
• *Alkalis are present in many household products:
– Liquid plumber, Drano, Oven cleaners, Glass cleaners (ammonia),
Dishwasher detergents, Lye, Drain openers, Alkaline batteries
 * Alkaline batteries are dangerous to children because they are
small and easily swallowed.
 * Alkaline dissolve tissues
– Liquefy membrane by interacting with proteins to form water
soluble salts & lipids through saponification
• * Solubilized cellular membranes
• - Protein, Na, K, Salt
• -Very penetrative & cause perforation
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Toxicity induced by household chemicals
1. Corrosive Alkalis
• * Penetrating effect:
-Least: sticking together of esophagus walls –stricture
• - Worst: perforation of membranes if swallowed
• ·At high dose Alkalis, can produce either an immediate death
to a delayed death
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• Acute effects:
• - Severe irritation of the eye, skin and other dermatoses
• Eye: disintegration and sloughing of the conjunctival and
corneal epithelium, corneal opacification, edema, ulceration)
• Skin: severe burn, deep skin ulceration, loss of hair
• mucous membrane: corrosion of the lips, mouth, tongue and
pharynx,
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Toxicity induced by household chemicals
1. Corrosive Alkalis
• Chronic effects:
  Esophageal strictures may occur in small doses, which can
lead to
respiratory distress.
  Burns (can be 1st to 3rd degree burns) causing skin scaring
  Permanent corneal opacification
  Dehydration which can lead to immediate death (From
traumatic shock and severe pain that leads to
cardiovascular
and
CNS collapse)
  Delayed death (24-48 hours later), (Due to internal injury
caused
by perforation)
  If the alkalis ingested is a small amount and make it into the
stomach, usually the acid will neutralize the toxin.
  If ingestion occurred, usually bloody emesis will be seen and
the patient will be unable to swallow so drooling may result.
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Toxicity induced by household chemicals
1. Corrosive Alkalis
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Management
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*Removal from exposure ASAP
*Flushing the eyes and skin with lots of water
*Use of an antibiotics ointment to prevent ocular adhesions
*Nothing should be given by mouth to dilute the poison
(unless the patient is in the act of swallowing)
• * If is already swallowed, give diluted vinegar or fruit juice to
balance GI pH, followed by administering eggs or
gelatin,
followed by stomach emptying where possible
• *Stomach intubation’s is not recommended because the
possibility of penetrating of the abdomen
• * If the alkalis were spilled onto the body, use Morphine to
reduce the pain and IV fluids should be given to reduce
shock
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Toxicity induced by household chemicals
1. Corrosive Alkalis
• * Treatments of esophageal stricture,
  Antibiotics (Penicillin or Ampicllin)
  Prednisolone to decrease inflammation of the esophagus
  Feed with a gastric tube 2-3 days after the ingestion
  Use special catheters (which have Mercury on the end which
slide
down the esophagus by gravity and do not have to be
pushed forcefully).
* Esophageal replacement:
– Previously, a portion of the colon was used
– Recently, a Reserve (inverted) gastric tube replacement is
performed
– A portion of the stomach is formed into a tube to act like the
esophagus (Continuity is not broken and the blood supply is not
interrupted)
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Toxicity induced by household chemicals
1. Corrosive Alkalis
• Batteries
• ·Alkaline
• · Toddler’s favorite are attracted to their size
• · If swallowed and there is no obstruction, the batteries will
not burst
and leak their contents
• · If the battery is excreted into the feces, no action should be
taken
• · Observe the child for 24-48 hours, if the battery is not
passed, then
an x-ray should be performed
• · If the battery is obstructed, the alkaline content may leak
and perforation may occur.
• · At this point, the battery should be removed by surgery
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Toxicity induced by household chemicals
2) Strong or concentrated Acids
• Source of exposure:
• - Any acid solutions used for cleaning brick,
garage (concrete) or bathroom floor
• - Acids will not affect the lipids of the
membrane, but will cause coagulation of the
proteins
• - The penetrative power is much less then the
alkalis
• - Acids produce more charring (burning) and
cause more pain
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Toxicity induced by household chemicals
2) Strong or concentrated Acids
Pathology
a) Acute Toxicity:
• - If ingested: ==►burning in the mouth, esophagus, stomach with pain,
nausea & vomiting
• - If inhaled: ==► coughing, burning in the throat, inflammation of the
nose, eye laryngeal spasms, pulmonary edema
• - Dermal: skin burn, dermatitis
b) Chronic Toxicity:
- Prolong exposure to diluted solutions ==►dermatitis, tooth erosion
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Toxicity induced by household chemicals
2) Strong or concentrated Acids
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Duration of Symptoms:
- 7-14 days depending or the rout of exposure
Treatment:
- Flush the skin, eye with H2O
- If inhalation is the rout, use 60-100 % O2
- For lung inflammation ==► use steroids (i.e. Prednisolone)
- For GI ==► use milk of magnesia (as an antacid and
laxative)
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Toxicity induced by household chemicals
3) Phenols
Source of Exposure:
- Disinfectants, (at homes, hospitals,
school,….), cleaning solutions
- Occupational exposure (manufactures,
packing, distribution, storage or use)
- In some skin medication, vaccine, inks
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Toxicity induced by household chemicals
3) Phenols
Pathology
a). Acute Toxicity:
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dark-colored urine
mucous membrane whiting
skin numbness, necrosis
GI disturbance
CNS effects
b). Chronic Toxicity:
- Similar to acute, but resulted from long term and
repeated exposure
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Toxicity induced by household chemicals
3) Phenols
• Duration of exposure:
• - If seizure developed ==► death due to respiratory OR
cardiac
collapse
• - If hepatic & renal failure developed ==►death occurs
after
several days
• Pathology:
• - esophagus appears tanned
• - cerebral edema
• - cardiac dilation
• - degeneration of glomerular and tubular cells of the
kidney
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Toxicity induced by household chemicals
3) Phenols
• Treatment:
• - Dermal: wash skin, eye with H2O (for at least 15
minutes)
• - If seizure developed ==►control with diazepam or
Phenobarbital
• - If ingested ==►Do not induce vomiting. Do not dilute
(may
absorption). Give polyethylene glycol solution
or activated charcoal with Sorbitol. wash stomach
repeatedly
with 25% bicarbonate
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Radiation Toxicology
• Source of Radiation:
• 1) Cosmic, radiation present in environment, radio active
materials in soil, rocks,….
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• 2) X-Ray diagnostics, dental, industry, T.V., industrial X-ray
machine, cobalt treatment for cancer, other 238PU
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3) Radioactive Pharmaceutics: used for diagnostic purpose
and/or
treatment (e.g., 131 I), in vivo or in vitro, in
RadioImmunoAssay
(RIA) kit
4) Reactors:
peace
time,
operate on the basis of nuclear fission, in
they produce energy and power
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Radiation Toxicology
Factors affecting toxicity:
1) Depend on the types of particles (α, Causing high degree of cell
damage, β or γ )
2) Dose and frequent of exposure
3) Whole body irradiation vs. partial exposure
4) Type of elements (radium, tritium)
5) t1/2
6) Tissue uptake and concentration
7) Type of tissue exposed
Toxic effects:
 - Radiation react with H2O to form free radicals
 - Free radical interact with cell molecules
- The result changing in cell function
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Radiation Toxicology
• Toxic effects:
* Radiation react with H2O to form free radicals
• * Free radical interact with cell molecules
 * The result changing in cell function
• Symptoms:
• * Anorexia, nausea, vomiting, diarrhea, apathy,
headache, fever, tachycardia, anemia
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Radiation Toxicology
• Delayed effects:
 * Mutation
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* Sterility
* Carcinogenesis
* Alopecia
* Shorten life expectancy (due to cancer)
* Cataract
• Treatment
 * Blood transfusions
• * Antibiotics
• * Supportive
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Radiation Toxicology
• Preventive measures
• * Don’t smoke, eat or drink while handling radioactive
materials
• * Wear protective clothes
• * No radiation exposure during pregnancy
• * Use Pb shield for X-ray
• * Keep distance from α, β
• * Every thing should be prepared under a designated
hood, disposed correctly
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Principle of Toxicology
December 2, 2011
Agents-Induced Toxicity
I. Natural Substances
• Animal source Fish (Puffer fish)
• Plant source (Wild Mushroom)
II. Heavy Metals
• Lead (Pb)
III. Drug of Abuse
• Amphetamine
• MDMA
• Cocaine
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Toxicity induced
Natural Substances
1) Animal Sources (fish)
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More than 700 species of marine fishes are
toxic (due to injury OR after ingested by
human):
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Some have tissue that are toxic at all times,
other are toxic at a specific period/areas and
some have specific organs that are toxic
Most potent marine toxin is Tetrodotoxin
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Toxicity induced Natural
Substances
1) Fish (Puffer fish)
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Fish-induced human
poisoning:
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Globe fish = puffer fish, contains a
potent and deadly toxin called
tetrodotoxin.
The toxin is concentrated mainly in
the eggs (ovaries), liver and skin.
The organs containing toxins even
after careful removal, there are still
chances that the flesh of the fish will
be contaminated.
The toxin cannot be destroyed by
drying, cooking, or freezing.
The toxin can affect a person’s
central nervous system, and in
extreme cases, can cause death.
There is no specific antidote at
present
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Toxicity induced Natural
Substances
1) Puffer Fish
Tetrodotoxin
– Is found in some puffer fish, amphibian species, octopus
– There are > 100 types of Puffer fish, (at least 50 are poisonous)
– Lethal dose is very steep (e.g., in mice):
• Minimal lethal dose = 8ug/kg
• LD99 = 12ug/kg
• Mechanism of Action:
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-blocks Na+ channels ( which are presents in every excitable tissue)
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- nerve and muscle blockade  paralysis
- produce hypotension & respiratory distress
- Tetraodotoxin can lead to death
- Many of the reported death in Japan was due to suicidal use of it
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Toxicity induced Natural
Substances
1) Puffer Fish
Clinical signs of Toxicity:
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Very rapid (5-30 min), muscle weakness  paralysis
Pallor
Numbness of the lips, tongue, throat (tingling or pricking)
 salivation
Change in HR (bradycardia, dyspnea, cyanosis shock 
death
Treatment:
– O2 & IV fluid (S Saline solution + dextrose)
– For the paralysis (due to  Ach) & Salivation  atropine
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Toxicity induced Natural
Substances
2) Plants (Mushrooms)
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Toxicity induced Natural
Substances
2) Plants (Mushrooms)
* Wild mushrooms induced different types toxicity in
human
1)
Mushroom produce GI discomfort & rapid nausea (w/in 3-4
hrs), emesis & diarrhea  dehydration, hypovolemic, shock
2) Mushroom-evoked sweating ( muscarine, not affected by
cooking), also may cause nausea & vomiting, blurred vision
3) Mushroom evoked Hallucination (symptoms appears + 2 hrs),
hyperthermia, loss of consciousness, severe symptoms =
alcohol intoxication
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Toxicity induced Natural
Substances
2) Plants (Mushrooms)
4) Mushroom-induced delirium/sleep & coma (symptoms w/in
20-90 min), w/in 60min  drowsiness, dizziness  sleep,
followed by  motor activities, tremor
5) Mushroom-induced disulfiram-like effects = alcohol intoxication,
headache, nausea & vomiting,pain (for up 3 days)
6) Mushroom-induce headache (delayed effect after 6-8 hrs,
onset
is sudden), may cause liver necrosis, pt recover w/in 26 days
7) Mushroom-induced polydepsia, polyurea (3 days later, lasts
3-17 days)
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Heavy Metals-Induced Toxicity
• Heavy metals:
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Lead (Pb)
Mercury (Hg)
Cadmium (Cd)
Arsenic (As)
Iron (Fe++)
Gold
Platinum
Beryllium
Chromium
Nickel (Ni)
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Heavy Metals-Induced Toxicity
Lead (Pb)
Source of exposure:
- Lead-based paints in older homes,
- household dust,
- drinking water (if you have lead pipes), and contaminated soil
- leaded gasoline
If lead accumulates
- Pb in the body mimics Ca++
- Pb will be stored in the bone like Ca++
- It has three compartments: Bone (t1/2 = 20-30 years), blood and
soft
tissue (t1/2= few weeks-3 mo)
- In children, more Pb is deposited in the bone due to growth
57
Heavy Metals-Induced Toxicity
Lead (Pb)
Acute Effects:
- when level > 50ug/dl  Pb encephalopathy
- If 60-80ug/dl in the blood, then seizures will develop
- infant, toddlers, young children are more susceptible to Pb than
adult
Chronic Effects:
If Pb in blood is 2-10ug/dl, no seizures but the patient will develop:
– Poor appetite, anemia
– ↓ attention span
– ↓IQ, ↓ memory
– Altered behavior
– Often mistaken for ADD
58
Heavy Metals-Induced Toxicity
Lead (Pb)
Pb at high dose may cause:
– Airway stricture
– Can produce death by local effect
– If patient survives initially, death can still occurs 2-3 days later
from Peritonitis
Management of Lead Poisoning (by Chelation)
- Succimer (DMSA) (chelating agent)
- Succinic acid, taken PO, and does not chelates Ca++ or Zn++
- British Anti Lewisite (BAL) for acute toxicity
- Ca++ Na2 EDTA
- Ca++ Na2EDTA + BAL  used when Pb in blood > 70ug/dl
59
Toxicity induced by
Drug of Abuse
• Drug of Abuse:
–
–
–
–
–
–
–
–
Amphetamine
Methamphetamine
MDMA
Cocaine
Cannabis (e.g., Marijuana, Hashish)
LSD
Nutmeg
Glue sniffing
60
Toxicity induced by Drug of
Abuse
1) Amphetamine
- A CNS stimulus, DA agonist
-Has limited therapeutic use (Narcolepsy)
Source of Exposure:
– Prescription over dose
– Illicit street drug
– Common route of exposure (PO, IV)
61
Toxicity induced by Drug of
Abuse
1) Amphetamine
Acute Toxicity: (CNS, CVS, GI):
1) CNS: Restlessness, dizziness, tremor, hyperactive reflexes, anxiety,
talkativeness,irritability, insomnia, confusion,
hallucination, panic
state, suicidal OR homicidal
tendencies, headache, seizure, coma
2) CVS: Cardiac arrhythmias, anginal pain, hypertension OR
hypotension, circulatory collapse, sweating
3) GI: dry mouth, metallic taste, anorexia, nausea, vomiting,
diarrhea, abdominal cramp
Chronic Toxicity: Same as acute symptoms, but more sever +
wt loss,
toxic psychosis, abnormal mental activities, 
dementia
62
Toxicity induced by Drug of
Abuse
1) Amphetamine
• Duration of Symptoms:
– Acute: for up to 2 hrs
– Chronic: 2-3 wks after withdrawal
– The Amphetamines cause psychological &
physical addiction
– They show cross tolerance with each other
and with stress
Pathology: Brain hemorrhage
63
Toxicity induced by Drug of
Abuse
Diagnosis:
1) Amphetamine
– History of Amphetamine use
– Detecting amphetamine & metabolites in urine
– Presence of any of the symptoms
Treatment:
– Emetic/Gastric lavage to remove drug from stomach
– Acidified the urine by ascorbic acid (urine pH<5)  
excretion of amphetamine
– If hypertension developed, use nitroglycerine, Na
nitrite to lower BP
64
Toxicity induced by Drug of
Abuse
2)M D M A
65
Toxicity induced by Drug of
Abuse
2) MDMA
MDMA
=
3,4, MethyleneDioxyMeth
Amphetamine
66
Toxicity induced by Drug of
Abuse
2) MDMA
MDMA
=
3,4, MethyleneDioxyMethAmphetamine
= Is known as designer drug
Street Names:
* Ecstasy
* E, *X,
* XTC
* Clarity
* Adam
* Stacy
67
Toxicity induced by Drug of
Abuse
2) MDMA
* It is an illegal drug
* Listed by DEA in
schedule I category of
the Controlled
Substance
68
Toxicity induced by Drug of
Abuse
2) MDMA
• Source of exposure:
– Street, illegal, available in tablet (50-100 mg) $20-25),
capsules, powder & liquid
– Distributed & used openly in bars & nightclubs in TX, AR &
southwest
– Could be purchased via toll-Free 800- number
– Sold in little bottles at convenient stores under the label
“Sassyfras” extracted from Sassyfras oil
– 80-90 % of the world MDMA manufactured in Belgium and
Holland
– Russian-Israeli & Eastern European chemists are now the main
producing and distributing of MDMA
69
Toxicity induced by Drug of
Abuse
Frequency of use:
USA:
–
–
–
–
–
2) MDMA
as of 2004, 11 Million age 12 Y and older used MDMA at least once
from 1995-2005, the use  970%
in 1993, 2% of all US college students used MDMA within 12 Month
In Stanford Univ, 39% of all undergraduate used MDMA at least once
MDMA use in 8th grade  by 52% & in 10th grade  58% &
in
12th grade  67%
International:
In England, 6% aged 14-15 & 31% aged 16-25 Y used MDMA,
500K-1 M used MDMA every weekend
– Widely used in Spain, Portugal, Australia, India,…
– 3% of all European adult had tried MDMA
70
Toxicity induced by Drug of
Abuse
2) MDMA
Acute effect: CNS, CVS, GI (w/in 30 min,  w=in 90 min))
(immediately after ingestion OR after the euphoric high subsided and
they tried repeated dosing OR co-ingestion with other drugs e.g.,
alcohol, marijuana, heroin, cocaine)
• Central nervous system
- Change in mental status, seizures
- Anxiety, paranoia
- Increased psychomotor activity, restlessness, Ataxia
- Hyperthermia, hot flashes
- Headache
- Blurred vision, halos
- Syncope
•
Cardiovascular (1/10 of Amph) Gastrointestinal/Urinary:
- Palpitations
- Dry mouth, Nausea & vomiting
- Chest pain
- Abdominal cramping, anorexia
- Urinary retention/sexual dysfunction
71
Toxicity induced by Drug of
Abuse
2) MDMA
Chronic Toxicity:
– Serotonin (5-HT) syndrome  hyperthermia, mental changes,
alter muscle tone and/or rigidity, hyponatremia ( Na+)
– Cerebral hemorrhage
– Hepatotoxicity, liver failure, alters liver enzymes
Long-term neuropsychiatric effects
due to permanent damage of the 5-HT system  depression,
anxiety, panic attack, insomnia, difficulty concentrating, shortterm memory impairment
72
Toxicity induced by Drug of
Abuse
Diagnosis:
2) MDMA
– History of drug use
– Detecting MDMA & metabolites (MDA) in urine
– Presence of any of the symptoms
Treatment:
– Emetic/Gastric lavage to remove MDMA from
stomach
– Cool room (environmental) to reduce hyperthermia
– Treat seizures with benzodiazepine.
– If hypertension developed, use nitroglycerine, Na
nitrite to lower BP
73
Toxicity of Drug of Abuse
3) Cocaine
Source of Exposure:
–
–
–
–
Most potent naturally occurring CNS stimulus
Alkaloid extract from Erythroxylun Coca
Sold as an illicit street drug
Street names e.g., coke, snow, flake, Cadillac or champagne of
drugs, gold dust, speedball (heroin+cocaine)
Abuse Pattern:
– Sniffing/snorting (chopped crystals into fine powder (t1/2=75
min)
– Smoking (Crack, tiny crystalline pieces in cigarette, water pipe)
(rocks, free –base cocaine in pipe) (t1/2= 45-48 min)
– IV: a combination with heroin (t1/2 = 50-55 min)
– 25 mg iv = 100 mg sniffing (Δ 15-20 min), PO (Δ 50-90 min)
74
Toxicity of Drug of Abuse
3) Cocaine
Medical Use:
– Mucous membrane anesthesia
– Vasoconstriction (2-4 min, ear, nose & throat surgery)
Acute Toxicity: CNS & CVS, Respiratory
CNS: Anxiety, headache, tremor, clonic & tonic, seizure, cold sweat
CVS: hypotension, weak & rapid pulse rate
Respiratory failure
Chronic Toxicity: Facial pallor, sunken eyes, tremor, Mydriasis
Duration of symptoms: death occurs 20-30 min after acute large
dose, recovery occurs 1-2 hrs after low-mild
dose
75
Toxicity of Drug of Abuse
3) Cocaine
Pathology:
– Cardiac dilation, sign of asphyxia, mal nutrition
Diagnosis:
– History of use
– Identification of the drug/its metabolites in urine
Treatment:
– Seizure  Diazepam (DOC), Short acting barbiturate (IV), 2nd choice
– Hyperthermia ice bath, hypothermic blankets, or cool room
– To control respiration  artificial respiration to maintain O2 content in
blood (ASAP)
76
Toxicity of Drug of Abuse
3) Cocaine
• Cocaine & Pregnancy:
– Cocaine Babies:
• New born babies to cocaine user mothers have
– Low birth weight
– Low (smaller) brain
– Increase malformation (birth defect)
– Low IQ, learning & memory
– Depression of interactive behavior
– Poor response to external stimuli
– Spontaneous abortion (e.g., after IV)
• Due to placenta vasoconstriction
• Due to uterine contraction
77