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Poison Source, Info Mechanism of Action Symptoms Treatment Antidote/Antito1) 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 antito

b) Bacterial (food) PoisoningSalmonella, 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, supportive2) 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) CarbamatesExample...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 furt

absorption

3) Herbicides:

a)Chloro-phenoxy Compoun

2,4-D; 2,4,5-T

(TCDD from forest

fires)

b) DinitrophenolsUncouple oxidative

phosphorylation

Incr. metab rate and incr. temp

c) Paraquat

"Paraquat Pot"once

used on marijuana

fields

none = death

4) Occupational Hazards

a) Halogenated Hydrocarbo

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 Alcoho

dehydrog = will decr

formation of methan

toxic metabolites) or

Fomepizole = synthe

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: 15

300mg%. Severe: 30

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 - prevent

glycol convert to oxa

acid via dehydr

competition. Fomepi

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.

Peri h vasoconstric = warm flushed skin**Disulfiram = inhibits acetaldehyde dehydrogenase = accum of acetald in blood = nausea,

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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) CorrosivesOxalic 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:

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, metabacidosis, shock

lavage ONLY w/in 1st hour after

ingestion, Deferoxamine

orally/parenterally, treat sx,

support

d) MercuryAll 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

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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 > affinitythan 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 dueto progressive brain anoxia.

Carboxy Hb is cherry red so

victims may have bright-red,

healthy looking mucous

membranes

terminate exposure immed, admin O2by 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 S

(excreted). Give artif

resp w 100% O2, tre

sx, support

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