Poison Source, Info Mechanism of Action Symptoms Treatment Antidote/Antitoxin

1) Household Poisons:
a) Botulinus Toxin (food)
Food-borne exotoxin...
heat-labile, but can
destroy by boiling
Block Ach release= blocks
impulses to muscles =
paralysis
8h-8d, vomiting, 2Xvision, musc
paralysis (intercostals,
diaphragm)
emesis, lavage, cathartic (depends on
ingestion time), support vitals, draw
for toxin levels,
ABE botulinus antitoxin
b) Bacterial (food) Poisoning
Salmonella, etc. (non-
living bact, ingest
finite toxin)
2-4hrs after-eat, severe GI
inflamm, mild fever, dehydr,
(shock)
anti-emetic (prochlorperazine) to
control vomit, fluids, supportive
c) Bleach
3-6% NaHCl in H2O Incr. w dose: severe irritation,
hypotens, delerium, coma (Cl
bleach = sever tissue damage if
ingested)
Clear skin by flood w H2O, DO NOT
USE EMESIS, LAVAGE, ACID
ANTIDOTES - makes gas, can
rupture tissues. Use milk, ice cream,
eggs, antactids, supportive
2) Agricultural Poisons:
a) Organo-phosphates
Examples... parathion,
malathion
Irreversible cholinesterase
inhibitors
SLUD, Mild: anorexia, HA,
dizzy, weak, anx, tounge/eye
tremor, miosis, visual acuity.
Mod: nausea, salivation, tear,
abd cramp, vomit, sweat, slow
pulse, musc fascic. Severe:
diarrhea, pin-point/non-reactive
pupils, resp diff, pulm edema,
cyanosis, coma, hrt block
remove contam clothes, wash skin, sm
dose atropine to block cholinergic
effect (incr. prn). 2-PAM can help
reactivate AChE, gastric lavage/emisis
if recent, support
SLUD: Salivation,
lacrimation, urination,
defecation
(cholinomimetic)
b) Carbamates
Example...Carbaryl REVERSIBLE
Cholinesterase Inhibitor
Same as organophosphates Same EXCEPT DON'T USE 2-PAM
c) Strychnine
rodenticide, but
rats=smart
Competitive ANTAG of
Glyc. Gly=inhib transmitter
to motor/interneurons in
spinal cord. Strych blocks
norm inhib of nerve
impulses = convulsions &
skel musc rigidity
Convulsions, very sensitive to
sensory stimuli. Death from resp
paralysis and failure
Support, IV Diazepam or
succinylcholine (NMJ inhibitor) for
convulsions.
Charcol prevents further
absorption
3) Herbicides:
a)Chloro-phenoxy Compounds
2,4-D; 2,4,5-T
(TCDD from forest
fires)
b) Dinitrophenols
Uncouple oxidative
phosphorylation
Incr. metab rate and incr. temp
c) Paraquat
"Paraquat Pot"once
used on marijuana
fields
none = death
4) Occupational Hazards
a) Halogenated Hydrocarbons
CCl4, chloroform,
methylene chloride,
cloroethylene,
triclethylene,
tetralethylene
Liver toxicity: CCl4 =
metab by cyto P-450 to free-
radical CCl3. Free rad-
induced lipid peroxidation
= Inc Intracell Ca = cell
death
CNS Depresents, can cause
arrhythmias at high doses by
sensitizing the myocardium to
catecholamine stimulation. May
cause LIVER and kidney damage
Remove contam clothes to stop further
absorb, treat sx, support
b) Alcohols and Glycols
Methanol Acute toxicity = rapid
metab to formaldehyde &
formic acid (in extracell
space, very charged)
visual probs (see snow falling),
metab acidosis. Death from
acidosis or respiratory failure
emesis, lavage, treat acidosis w
NaBicarb
50% Ethanol IV
(compete for Alcohol
dehydrog = will decr
formation of methanol's
toxic metabolites) or
Fomepizole = synthetic
alcohol dehydrog
inhibitor = expensive
Ethanol
Acute: support, avaoid depress drugs,
hemodialysis if blood levels
>500mg%. Chronic: treat seizures
assoc w alcohol w/d, IV Diazepam,
addict/fam counsel
Acute = BAC5 50-
150%. Moderate: 150-
300mg%. Severe: 300-
500mg%. Coma
>500mg%
Isopropyl (rubbing)
Alcohol
CNS depression - like other
alcohols, renal damage
gastric lavage, treat sx
Ethylene & diethylene
glycol
same + kidney damage due to
calcium oxalate crystals (acidosis
ppt)
gastric lavage, sx, support Ethanol IV - prevents
glycol convert to oxalic
acid via dehydr
competition. Fomepizole
c) Hydrocarbons Petroleum distillates
mixes of aliphatic
hydrocarbons like kerosine,
diesel fuel and gasoline,
white spirit, polishes
pulm irritation by high conc of
vapor, CNS depress by ingest or
inhale, severe pneumonitis after
aspiration of liquid
sx and support,
CONTRAINDICATED: emesis and
gastric lavage w/o tracheal intub
High doses = signs of neuromusc involv. Often contam w TCDD = extrem toxic in some species, NOT MUCH IN HUMANS.
TCDD ? reproduct or carcinogen probs w/ lg amts for long time
Undergoes redox cycling & causes free radical-mediated
injury to lungs
CNS: stim due to inhib of CNS inhib path (GABA), then
anaesthetic-like CNS depression at higher doses, visual
impairment, musc incoord, slow rxn time, euphoria, resp
depress, coma. Kidney: diuresis by ADH inhibit, temp +
fluid bal. Incr salivation, gastric secretion = incr appertite.
Periph vasoconstric = warm, flushed skin
**Disulfiram = inhibits acetaldehyde dehydrogenase = accum of acetald in blood = nausea,
vomiting
Aromatic
Hydrocarbons
benzene, toluene, xylene CNS stim at low doses or early in
high doses then CNS depress in
more serious cases. Kidney and
liver damage after high acute
doses or prolonged exposure.
Arrhythmias from catecholamine
release from high exposures.
Long term exposure to benzene
can caus eaplastic
anemia/leukemia
remove ingested hydrocarbon by
gastric lavage ONLY if aspiration can
be prevented. DO NOT induce emesis.
Control excitement/convulsions with
IV Diazepam
d) Corrosives
Oxalic Acid and
oxalates
local irritation/corrosion of GI,
muscle weak, convulsions,
collapse from Ca chelation.
Renal tubular damage from Ca-
oxalate ppt
ppt oxalate in GI by giving Ca in any
form (milk..). Monitor renal funct,
force fluids to prevent oxalate crystals
from depositing in kidney tubules. DO
NOT USE gastric lavage/emesis
Antidote = specific: Ca
gluconate IV
Mineral Acids
hydrochloric, sulfuric,
acetic, perchloric
irritat, inflamm and/or necrosis in
all of GI exposed to corrosive.
Death = from unresolved
hypovolemic shock after massive
hemorrhage.
DO NOT USE gastric lavage/emesis
after ingesting acid. Dilute acid with
H2O, analgesics for pain, sx, support
non-specific: milk of
magnesia
Strong Alkali
hydroxides in soaps,
cleaners
irritate, inflamm, tissue damage.
MORE PENETRATING THAN
STRONG ACIDS. Death =
hypovolemic shock
DO NOT USE gastric lavage/emesis.
Dilute alkali with H2O, treat sx,
support
5) Metals
a) Arsenic and arsine
many chem forms toxicity from binding to
sulfhydryl groups on
enzymes, interfering w cell
metab
ACUTE: GI prob, CNS-
convulsions, coma = terminal
signs, ventricular arrhythmias,
kidney tubular damage.
CHRONIC: polynephritis,
nephritis, dermatitis, cardiac fail,
liver cirrhosis, personality
changes
remove via lavage/emesis.
Dimercaprol or penicillamine =
chelators, treat sx
b) Lead
One of most toxic
metals b/c accum in
body. Greatest degree
= children. Lead is
stroed in bone, but sx
are due to lead in soft
tiss like BM, nerv syst
tiss
Treat: remove unabsorbed lead, sx.
Chelation forms the organic form =
more likely to cross the BBB.
However, w/ SEVERE CNS toxicity =
CHELATION MUST BE USED
c) Iron
Fe is highly charged,
but with GI damage
you can absorb lots!
Severe GI irritation,
inflamm, necrosis and
hemorrhage (mucosal block
is destroyed) resulting in
hypotension, metab
acidosis, shock
lavage ONLY w/in 1st hour after
ingestion, Deferoxamine
orally/parenterally, treat sx,
support
d) Mercury
All Mercury salts =
toxic
Many effects of acute
poisoning are related to GI
tract damage.
Inorganic Mercury
Acute: irritate/superficial
corrosion, abdom pain, vomiting
(?blood). 2ndary: diarrhea, acute
renal tubular necrosis, shock.
Delayed: severe kidney damage
leading to anuria, sever GI
damage and hemorrhage.
Chronic: (early) salivation,
stomatitis - swollen, bleeding
gums, rarely "mercury line" on
gums. (late) erethism - emotional
instability, tremor, stomatitis
(more severe, may lose teeth).
Continued exposure: coarse,
jerky extremities, drowsiness,
depression, memory loss,
hallucinations, delusions, mania
"Mad Hatter"
lavage or induce emesis. Give milk,
raw eggs or charcol. Dimercaprol
parenterally for inorganic mercury
(NOT ORALLY) b/c chelated form is
more readily absorbed from the GI
tract. Treat sx, support
Organic Mercury (methyl
and tetraethyl mercury -
more lipid soluble)
Predominantly CNS effects:
paresthesia, muscle twitching,
ataxia, gross constriction of
visual fields
ACUTE: GI irritate, kidney damage.** acute more likely to
get into CNS. **CHRONIC (plumbism): lead line on gums,
basophil RBC stippling (=immature RBCs from presence of
RNA in cells), accum aminolevulinic acid (Hb precursor) from
inhibit of heme synth by Pb. GI (lead colic): anorexia,
constipation, abdom pain. CNS effects (in kids - BBB more
permeable). Hyperirritability: behav disturbs, intellect deficits,
loss of recently developed skills, finally coma and
incontractable convulsions. Neuromusc effects: weak,
paralysis, incoord, arthralgia, "wrist/ankle-drop" b/c of
Nitrites
Directly induce MetHb =
incapable of carrying O2
choc-colored blood, hypotension,
hypoxia, cyanosis, convulsions,
coma, resp failure
Only need treat if >35% of Hb is in
the oxidized (un-usable) form.
Methylene blue will convert MetHb
back to Hb through its effect on an
intraRBC enzyme reduction mech. In
severe cases, O2 administration and
exchange transusions are helpful
Carbonmonoxide
odorless, colorless gas.
One of the most frequ
causes of lethal
poisonings in the USA
CO has much > affinity
than O2 for Hb (X200) and
carboxyHb cannot transport
O2. Also impairs the ability
of OxyHb to give up its O2
to peripheral tissues
HA, dizzy, stupor primarily due
to progressive brain anoxia.
Carboxy Hb is cherry red so
victims may have bright-red,
healthy looking mucous
membranes
terminate exposure immed, admin O2
by best means avail, AVOID resp stim
drugs inlcuding CO2, DO NOT GIVE
methylene blue. Treat sx, support
Cyanide
colorless gas w a
penetrating odor
resembling almonds
complexes w ferric iron of
cytochrome oxidase and
produces cellular anoxia by
inhibiting O2 utilization in
the mito. It is one of the
most rapid acting poisons
and death can occur very
rapidly after exposure.
Dizziness, HA, hypotension,
unconciousness, convulsions,
resp fail
MUST BE RAPID, administer Na-
nitrite or amyl-nitrite to form MetHb.
MetHb competes w very sensitive
cytochrome oxidase for the cyanide
ion. Cyanide is normal in body in
extremely sm amts, normal biochem
syst for excretion involves Rhodanese.
Since Sulfur is the limiting co-factor,
Na-thiosulfate is given IV immed after
nitrite admin.
Rhodanse = CN- + S
(thiosulfate) yields SCN-
(excreted). Give artifical
resp w 100% O2, treat
sx, support
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ulmercaprol
8AL: 8rlush Anu-
LewlslLe
arsenlc, lead, gold,
lnorganlc mercury
CnS dlsLurbances, Cv dlsLurb
(may produce shock due Lo
caplllary damage), 8AL-lron
complex = Loxlc, Lhus avold
medlclnal lron durlng 8AL
Lherapy
7-10 days by deep lM ln[ecuon.
Can be used wlLh vlrLually
compleLe renal shuLdown.
Calclum ulsodlum LdeLaLe
Cana2Lu1A Lead, Zlnc, AlLernaLe
cholce for oLher meLals
8enal damage, LkC
abnormallues, Loxlc eecLs
can be avolded by uslng less
Lhan 30mg/kg/day
urlne ow musL be malnLalned,
Lherapy should noL exceed 3-7
days, uC nC1 uSL na2Lu1A b/c
wlll blnd Ca, causlng
hypocalcemla
enlclllamlne
Copper, AlLernaLe cholce
for oLher meLals
nephrouc syndrome,
pyrldoxlne declency,
LranslenL eoslnlophllla,
CCn18AlnulCA1Lu ln klds w/
chronlc renal lnsumclency
Succlmer
ueferoxamlne
l8Cn (lngesLed) rapld lnfuslon may lnduce
shock, long-Lerm Lherapy may
cause ocular damage
oral dose ls eecuve ln blndlng lL
ln Lhe Cl
Chemlcal compounds LhaL blnd meLals ln sLable complexes Lo be excreLed ln Lhe urlne or feces
Llke ulmercaprol, buL can be glven orally. MosL common S/L = Cl dlsLurbances
Agents that Affect Heme Proteins